
asssssas* c^csr »=: 










































































































COFYHIGHT DEPOSIT. 









DISEASES OF THE EAR 


BY 

PHILIP D. KERRISON, M.D., 

AURAL SURGEON TO THE WILLARD PARKER HOSPITAL FOR INFECTIOUS DISEASES! JUNIOR 
AURAL SURGEON TO THE MANHATTAN EYE AND EAR HOSPITAL; FELLOW OF THE 
AMERICAN COLLEGE OF SURGEONS; MEMBER OF THE AMERICAN OTOLOGICAL 
SOCIETY; AMERICAN LARYNGOLOGICAL, RHINOLOGICAL AND OTOLOGICAL 
SOCIETY; AMERICAN ACADEMY OF OPHTHALMOLOGY AND OTO¬ 
LARYNGOLOGY; NEW YORK OTOLOGICAL SOCIETY AND 
NEW YORK ACADEMY OF MEDICINE 


332 ILLUSTRATIONS IN TEXT 
AND 2 FULL PAGES IN COLOR 


Third Edition—Revised and Enlarged 



o > ) 

> 1 


PHILADELPHIA U LONDON 

J. B. LIPPINCOTT COMPANY 





. K4U 


COPYRIGHT, 1913, BY J. B. LIPPINCOTT COMPANY 
COPYRIGHT, 1921, BY J. B. LIPPINCOTT COMPANY 
COPYRIGHT, 1923, BY J. B. LIPPINCOTT COMPANY 


OCT 2V> 1923 


> « 

) >» 
' :> 9 


PRINTED BY J. B. LIPPINCOTT COMPANY 
AT THE WASHINGTON SQUARE PRESS 
PHILADELPHIA , U. S. A. 



\ » 


©C1A739574 


PREFACE TO THE THIRD EDITION. 


The purpose of successive revisions of a medical text book is 
naturally to make it as nearly representative, as the writer’s ability 
permits, of whatever is significant in recent thought or research. 

While the comparatively rapid exhaustion of the second edition 
has made any re-writing of chapters—had that been advisable—out 
of the question, a conscientious effort has been made to interpolate 
whatever of recent work has been of approved interest or value. The 
new matter has been carefully indexed, and it is hoped that these 
additions, with the bibliography relating thereto, may give to this edi¬ 
tion a greater value as a practical book of reference. 

The relatively recent studies and writing of Dr. A. A. Gray of 
Glasgow on the nature and pathology of oto-sclerosis and the wide¬ 
spread revival of Anglo-Saxon interest resulting therefrom, the 
developing theories as to the physiology of the so-called “otolith 
mechanism,” now under investigation by the Dutch School of 
Otologists, the renewed interest of our British collegues in the con¬ 
flicting theories of tone perception, and the obvious tendency toward 
a broader neurologic investigation of intracranial lesions of otitic 
origin' give to the student and practitioner of otology much food 
for stimulating thought and speculation. 

One new chapter—on Tumors of the 8th Nerve —represents an 
extension of the field usually covered by text books on otology. 

With the constantly broadening concept of medical science as a 
whole, the merging or overlapping of related branches has been one 
of the most conspicuous tendencies of recent years. As neurology 
has borrowed and assimilated the results of Baranv’s work on the 
physiology of the labyrinth, so of necessity has otology been forced 
at certain points to invade the domain of neurology. 

In a relatively recent paper, a distinguished surgeon, speaking of 
tumors of the acoustic nerve, brought otologists under the implied 
reproach of having usually failed with respect to this lesion even “to 
recognize the presence of a tumor at all.” Clearly, this statement, 
or its implications, if justified, would bring discredit upon otology. 
If we accept the fact that the eighth nerve, quite as much as the drum 
membrane or ossicles is part and parcel of the organ or mechanism 



PREFACE TO THE THIRD EDITION 


of hearing, it is clear that a working knowledge of this veiy grave 
lesion should not be confined to special students of oto-neurology, but 
should belong quite generally to the rank and file of otologists. Lack 
of such knowledge may lead an otherwise competent aurist into serious 
errors of diagnosis and treatment. 

The author believes that no addition to this book could be of 
greater interest or value to practical otologists than a chapter giving 
in condensed form the accepted facts as to the incidence, gross path¬ 
ology, prognosis, and particularly as to the symptomatology, of tumors 
of the eighth nerve. 

The Author 


June, 1923 . 


PREFACE TO SECOND EDITION 

While the past few years have been marked by no startling develop¬ 
ments in otology, advances of a practical order have not been wholly want¬ 
ing. Our conception of the pathology, processes of repair and rationale of 
treatment of certain lesions has undergone very considerable modification. 
The mastoid operation of a few years ago was a bone operation pure and 
simple. To-day the plastic work vies in practical importance with that 
upon the temporal bone itself. In other words, our conception of the 
important role which the soft parts may play in post-operative tissue 
repair has led logically to a different surgical technic, which, in turn,, 
has given us better and quicker results. To record these developments 
parts of this chapter have been practically rewritten. Again, the further 
study of the changes in the cerebrospinal fluid occurring in various 
diseases has conduced materially to a more correct interpretation of the men¬ 
ingeal lesions and disorders of otitic origin and has brought to light certain 
sources of error in diagnosis. Beyond such changes and additions as were 
necessary to bring these practical phases of otology in line with modern 
ideas, alterations in the text and arrangement of the subject matter have 
been avoided. 

Two new chapters have been added, of which the first is devoted to 
Barany’s theory of the cerebellar control of joint movements, with a dis¬ 
cussion of the pointing tests in their relation to vestibular and cerebellar 
disease. The second includes a brief account of the various types of war 
deafness,—deafness due to direct injury of the skull, nerve deafness due to 
loud explosive noises, concussion deafness due to the air displacements of 
near-by explosions, psychic disturbances of function, pithiatism, etc.,—phe¬ 
nomena which constitute for most of us a practically new chapter in aural 
disease. Direct products of military hardship and injuries, as these lesions 
and functional disorders undoubtedly are, their relation to certain phases of 
some of the commoner ear lesions is sure to provide a fruitful field for future 
investigation and discussion. It is hoped, therefore, that the changes and 
additions which distinguish this edition from the first may prove to be of 
distinct practical usefulness to students and practitioners of otology 

Philip D. Kerrison. 





















I f" I III 













II 






a imm 
















. • 










. 















PREFACE 


Probably in no branch of medicine have more notable advances been 
achieved during the past decade than in otology. The wholly new field 
of work which has been opened to us by the successful investigation of the 
static labyrinth; the new light upon syphilitic lesions of the labyrinth and 
auditory nerve resulting from the recent world-wide renewal of interest 
in the study of all phases of syphilis; and the investigations still in 
progress as to the influence of autogenous vaccines and leucocyte extracts 
upon certain phases of aural disease,—these and other additions to our 
knowledge have suggested new problems in the working out of which 
laboratory investigations have been closely followed by practical thera¬ 
peutic results. 

In aural surgery our activities can no longer be confined to the narrow 
limits of the tympanum and mastoid process, but must include the more 
hazardous field of intracranial surgery and the yet more delicate and 
difficult work upon the auditory labyrinth itself. There is, then, some 
justification at the present time for yet another book,— i.e., an attempt to 
present the complex subject of otology in the light of recent advances. 

If the arrangement of the subject matter, particularly as to the pro¬ 
portionate space given to the different subjects, represents a departure 
from that usually followed, this has become necessary in order to bring 
the various subjects now pertaining to otology into a true relation with 
their actual and proportionate importance. 

For example, labyrinthine physiology, suppurative diseases of the 
labyrinth, and the surgery of the labyrinth, which are usually rather 
briefly dealt with, are here considered in three separate chapters which 
occupy a very considerable section of the book. Again, the suppurative 
lesions of the brain and meninges are accorded far more space than is 
usually allotted them in text-books of otology. 

In the Section devoted to operative surgery, the plan of illustrating 
each successive step of the various operations has been adopted. This, 
it is believed, will be of special value to students of otolog}^ living at a 
distance from the larger medical centres and who are therefore denied the 
educational advantages of large surgical clinics. With few exceptions, 
the illustrations throughout the book are from original drawings made 
under the writer’s personal supervision. 


PREFACE 


In the preparation of this manual the writer has endeavored to give 
greatest prominence to the practical side of otology. This has necessitated 
the elimination of many time-honored but discarded theories and thera¬ 
peutic measures which no longer have any bearing upon the practice of 
otology. 

In conclusion, I wish to express my thanks to Dr. J. IT. Guntzer for 
many valuable abstracts from the literature, and to Miss Eleanor Fry, 
whose clever and anatomically correct drawings form so attractive and 
valuable a feature of this book. I wish also to express my indebtedness to 
the publishers, Messrs. J. B. Lippincott Company, for many helpful sug¬ 
gestions as to the arrangement of the text. 


Philip D. Kerrison. 


CONTENTS 


CHAPTER I 

PAGE 


Anatomy and Physiology of the Sound Conducting Apparatus. 

The Auricle. 

Muscles of the Auricle. 

The External Auditory Meatus.. 

Development of the Osseous Meatus. 

Post-natal Changes.. 

The Osseous Meatus. 

The Tympanum. 

The Inner Wall. 

The Superior Wall. 

The Anterior Wall. 

The Posterior Wall. 

The Inferior Wall. 

The External Wall .. 

The Annulus Tympanicus. 

The Drum Membrane. 

The Ossicles.^.. ... 

The Malleus. 

The Incus. 

The Stapes. 

Shrapnell’s Membrane. 

The Ossicles, Their Articulations and Relative Positions Within the 

Tympanum. 

The Malleus. 

Ligaments of the Malleus. 

The Incus. 

Articulations of the Malleus and Incus. 

The Incudo-stapedial Joint. 

Articulation of the Stapes with the Fenestra Ovalis. 

The Intra-tympanic Muscles. 

The Stapedius. 

The Tensor Tympani Muscle. 

The Lining Membrane of the Tympanum. 

The Pouches, or Pockets, of the Membrana Tympani. 

The Attic Spaces. 

Vascular and Nervous Supply of the Tympanum. 

Arteries.. 

Veins. 

Nerves. 

The Eustachian Canal . 

The Osseous Portion of the Eustachian Tube. 

The Membrano-cartilaginous Portion of the Eustachian Tube. . . . 
Anatomical Differences Between the Eustachian Tubes of the 

Adult and the Infant at Term. 

Muscles of the Eustachian Tube. 

The Mastoid Process. 

The Pneumatic. 

The Diploic Mastoid.. 

The Antrum. 

Physiology of Sound-conduction. 

The Pitch. 

Intensity. 

Timbre. 


1 

1 

2 

3 

4 

7 

8 
9 

11 

12 

13 

14 

14 

15 

16 
16 
16 
16 
18 
18 
20 

20 

21 

21 

22 

22 

23 

23 

23 

23 

24 
24 
24 
26 
26 
26 
27 

27 

28 
28 

29 

30 

31 

31 

32 
32 
32 
34 

34 

35 
35 


Vll 




















































Vlll 


CONTENTS 


Sound-conduction. 35 

Auricle and External Auditory Meatus. 35 

The Drum Membrane. 36 

The Ossicular Chain. 37 

The Tympanic Muscles. 39 


CHAPTER II 


Physical Examination of the Patient. ... 41 

Age, Occupation, Habit, Heredity. 41 

Previous History. 41 

History of the Present Attack. 41 

Objective Examination. 42 

Auricular Displacement. 43 

Palpation in Case of Postauricular (Edema. 43 

Palpation of the Auricle in Case of Aural Pain. 44 

Inspection of the Drum Membrane. 44 

The Source of Light. 49 

Technic of Objective Examination; Landmarks of the Normal 

Drum Membrane. 50 

Landmarks of the Normal Drum Membrane. 53 

Examination of the Eustachian Tubes. 60 

Valsalva’s Method of Inflation. 60 

Politzer’s Method of Inflation. 61 

Inflation Per Catheter. 63 

The Nose, Nasopharynx, and Throat. 69 

Examination of the Nose. 70 

The Throat. 70 

Posterior Rhinoscopy. 71 


CHAPTER III 


Functional Examination of the Cochlear Apparatus; Hearing Tests. 

Air Conduction and Bone Conduction of Sound. 

Normal Hearing Distances for the Watch-tick, the Acoumeter, the 

Conversational Voice and Whisper. 

The Watch-tick... 

Politzer’s Acoumeter. 

The Conversational Voice and Whisper. 

Recapitulation. 

Changes in the Tone Limits. 

Loss or Impairment of Hearing for the Lower Musical Tones. 

Loss or Impairment of Hearing for the Higher Tones of the Mus¬ 
ical Scale.. 

Changes in the Period of Hearing by Bone Conduction 
Increase.. 

Diminished Hearing by Bone Conduction. 

Method of Examination. ’’’’’’ 

Watch and Acoumeter. 

Whispered and Conversational Speech... ' * ' * 

Determination of the Lower Tone Limit. 

Determination of the Upper Tone Limit. . . ’ ’ ^ ] ’ ’ ’ ’ ’ ’ ] [ [ 

Changes in Hearing by Bone Conduction 
Total Deafness. 


73 

73 

74 
74 

74 

75 

76 
76 

76 

77 
77 
77 

79 

80 
80 
81 
83 
86 
87 
91 


CHAPTER IV 

Diseases of the External Ear (Auricle; External Auditory Meatus) 

Inflammatory Diseases of the Auricle. 

Traumatic Auricular Dermatitis. 

Treatment.. 

Erysipelas of Auricle. 

Treatment. 


97 

97 

97 

97 

97 

97 





















































CONTENTS 


IX 


Frost-bite. 

Treatment. 

Auricular Eczema. 

Etiology.. 

Symptoms of Acute Auricular Eczema. 

Treatment. 

Chronic Eczema of the Auricle. 

Treatment. 

Auricular Perichondritis.. 

Symptoms... 

Terminations... 

Treatment. 

ELematoma Auris (Oth.ematoma). 

Etiology. 

Symptoms. 

Terminations. 

Treatment. 

Lupus. 

Treatment. 

Lupus Tumidus (Lupus Hypertrophicus). 

Treatment. 

Syphilis of the Ear. 

Herpes Zoster Auriculae; Herpetic Inflammation of the Genicu¬ 
late Ganglion (Hunt). 

Malignant Disease of the Auricle; Epithelioma; Cancer of the 

Auricle. 

Inflammatory Diseases of the External Auditory Meatus. 

Acute Circumscribed External Otitis. 

Etiology. 

Symptoms. 

Physical Examination. ... 

Course of the Disease. 

Prognosis. 

Treatment. 

Acute Diffuse External Otitis. 

Causes.. 

Symptoms. 

Treatment. 

Otomycosis. 

Etiology..... 

Symptoms. 

Treatment.. 

Croupous External Otitis (Otitis Externa Crouposa). 

Etiology. 

Symptoms. 

Treatment... 

Obstructive Conditions of the External Auditory Meatus. 

Foreign Bodies in the Meatus.• .. 

Removal of a Foreign Body by Means of the Syringe. 

Cases Requiring the Use of Instruments. 

Removal of Cerumen from the Meatus. 

Exostoses of the Osseous Meatus; Bony Outgrowths from the 

Walls of the Bony Canal. 

Treatment. 


98 

98 

98 

98 

99 
99 

100 

100 

101 

101 

101 

101 

102 

102 

103 

103 

103 

104 

105 
105 
105 

105 

106 

107 

107 

107 

107 

108 
108 
109 
111 
111 
116 
116 
116 
116 
117 
117 
117 

117 

118 
118 
118 
118 
119 
119 

119 

120 
123 


125 

125 


CHAPTER V 

Causes of Acute Tympanic Disease .. 

Predisposing Causes. 

Age... 

Nasal Obstruction. 

Exciting Causes. 

Acute Rhinitis. 


126 

126 

126 

126 

127 

127 



























































X 


CONTENTS 


Acute Infectious Diseases. 127 

External Causes. 129 

Occupations and Habits as Causes of Aural Disease. 130 


CHAPTER VI 

The Subjective Symptoms op Aural Disease. 133 

Aural Pain. 133 

Pain in Acute Otitis Media. 133 

Pain in Chronic Catarrhal Otitis Media. 133 

Pain in Furunculosis of the Meatus. 134 

Reflex Aural Pain. 134 

Impairment of Hearing. 134 

Aural Discharge. 135 

Discharge in Acute Otitis Media. .. 135 

Discharge in Chronic Suppurative Otitis. 135 

Tinnitus Aurium. 136 

Obstruction Sounds. 136 

Blood Sounds. 138 

Labyrinthine Sounds. . 140 

Neurotic Sounds. 141 

Cerebral Sounds... 143 

CHAPTER VII 

Acute Inflammatory Diseases of the Eustachian Tube, Middle Ear, and 

Mastoid Process. ... 145 

Acute Tubal Catarrh; Eustachian Catarrh; Tubctympanic Conges¬ 
tion. 145 

Tubal Catarrh. 145 

Etiology. I45 

Pathology. 145 

Symptoms. 146 

Physical Signs. 147 

The Course of the Disease. 148 

Prognosis. 149 

Treatment.■. 149 

Tubal Catarrh in Children.’ ’ ’ 153 

Absence of Subjective Symptoms. 155 

Physical Examination. 155 

Treatment. 255 

Myringitis.’ 2 59 

Acute Middle-ear Inflammation.157 

Nomenclature: Significance of Names in Common Use.* ] ’ ’ ’ 157 

Otitis Media Catarrhalis Acuta; Acute Catarrhal Otitis Media.. ! 158 

Etiology. 258 

Anatomical Conditions in Relation to Symptoms.160 

Symptoms and Signs.[ 160 

Prognosis.265 

Acute Suppurative Otitis Media; Acute Purulent Otitis Media 

(Otitis Media Purulenta Acuta). 165 

Etiology.’ ’ 265 

Anatomical Conditions Influencing the Pathology of the 

Disease... 165 

Symptoms and Signs.166 

Complications of Acute Purulent Otitis Media. 170 

Treatment.. .. 271 

Acute Mastoiditis. '' .. 281 

Etiology... 281 

Pathology. . 281 

Symptoms.’ ’ ’ ’ . 283 

Prognosis.’ ’ ’ . 288 

Treatment.. 188 






















































CONTENTS 


xi 


CHAPTER VIII 

Chronic Middle-ear Suppuration. 292 

Otitis Media Purulenta Chronica. 292 

Etiology. 292 

Pathology. 292 

Symptoms and Signs ..’ ' [ ’ ’ ' ’ ’ ’ ’ ’ ’ ’ ’ ’ 298 

Diagnosis.^ 200 

Complications. 205 

Treatment. 205 

CHAPTER IX 

C hronic Non-suppuratiye Diseases of the Middle Ear; Otosclerosis. 219 

Chronic Tubal Catarrh. 219 

Nasal Obstruction. 221 

Chronic Tubal Congestion. 221 

Treatment. 222 

Structural Narrowing of the Tube. 222 

Chronic Non-suppurative Tympanic Disease.223 

Chronic Hypertrophic Otitis Media.. . 223 

Etiology. 223 

Pathology. 223 

Symptoms. 224 

Physical Signs. . . . ’ ’ ] ’' 226 

Prognosis. 229 

Treatment. 229 

Chronic Hyperplastic Otitis Media. 234 

Symptoms. 235 

Physical Appearances of the Drum Membrane. 236 

Course of the Disease; Prognosis. 238 

Treatment. 238 

Otosclerosis. 244 

Etiology. 244 

Pathology. 245 

Symptoms and Diagnosis.<.. 250 

Otosclerosis with Involvement of the Cochlea. 253 

Symptoms. 253 

Otosclerosis Complicated by Chronic Catarrhal Otitis Media. ... 255 
Treatment. 255 

CHAPTER X 

The Anatomy and Physiology of the Labyrinth. 260 

The Osseous Labyrinth. 260 

The Membranous Labyrinth. 265 

Physiology of Sound Perception (Cochlear Function). 274 

CHAPTER XI 

Inflammatory and Suppurative Lesions of the Labyrinth. 278 

Ewald’s Experiments. 278 

Barany’s Experiments; The Caloric Reactions . . .. 280 

Vestibular Nystagmus. 281 

Physiological Nystagmus. 283 

Rotation or Turning Experiment. 283 

The Symptom Complex of Vestibular Irritation: Nystagmus, Ver¬ 
tigo, Ataxia. 287 

Suppurative Labyrinthitis. 292 

Diffuse Suppurative Labyrinthitis. 292 

Etiology. 292 

Symptoms. 294 

Terminations; Prognosis. 309 

Circumscribed Suppurative Labyrinthitis. 309 

Symptoms. 310 






















































XU 


CONTENTS 


Diffuse Serous Labyrinthitis. 310 

Perilabyrinthitis.. 312 

Symptoms. 312 

Acute Hyperemia of the labyrinth. 313 

Prognosis and Treatment of Diffuse Suppurative Labyrinthitis. . 313 

Treatment of Circumscribed Suppurative Labyrinthitis. 318 

Treatment of Diffuse Serous Labyrinthitis. 320 

Treatment of Perilabyrinthitis. 320 

CHAPTER Nil 

Symptoms of Intracranial Disease Secondary to Aural Suppuration. 322 

Headache. 322 

Vomiting. 323 

Temperature Changes. 324 

Changes in Pulse Rate. 325 

Unilateral Muscular Spasm as a Symptom of Cerebral Disease.326 

Unilateral Muscular Paralysis or Paresis. 327 

Mental Disturbances. 330 

Aphasia... . 331 

Sensory Aphasia. 334 

Motor Aphasia. 336 

Motor Agraphia,. 336 


CHAPTER XIII 

Intracranial Lesions of Otitic Origin: Extradural Abscess; Perisinous 
Abscess; Septic Sinus Thrombosis or Phlebitis; Purulent Lepto¬ 
meningitis; Cerebral Abscess; Cerebellar Abscess.. 337 

Avenues of Infection... ’ 337 

Extradural Abscess; Epidural Abscess. 338 

Etiology. 333 

Symptoms. 338 

Prognosis.. 339 

Perisinous Abscess and Infective Sinus Phlebitis. 340 

Perisinous Abscess. ’ ’ ’ 349 

Symptoms. 342 

Prognosis. 343 

Infective Sinus Phlebitis; Suppurative Thrombophlebitis of the 

Sigmoid or Lateral Sinus; Sigmoid Sinus Thrombosis. 343 

Etiology. 344 

Pathology. ’ ’ ’ ’ ’ ‘ 344 

Symptoms.. . 345 

Prognosis. . or a 

1 reatment. 355' 

Abscess of the Brain. .357 

Etiology. ’ .357 

Pathology. . 

Symptoms. qao 

Prognosis. 375 

Cerebellar Abscess.• .... .375 

Symptoms. 3^ 

Differential Diagnosis. 379 

Otitic Meningitis. .332 

Circumscribed Pachymeningitis.. 332 

Leptomeningitis. .3§2 

Diffuse Purulent Leptomeningitis. 383 

Paths of Infection. . 000 

SYMPTOMS. qqq 

Prognosis. 385 

Circumscribed Leptomeningitis. . 335 

Serous Meningitis; Serous Meningoencephalitis (Korner! as7 

Meningismus.;. . . oju. 

Differential Diagnosis .. ooq 

Treatment. . 
























































CONTENTS xiii 

CHAPTER XIV 

Barany’s Theory of Cerebellar Centres: Normal Accuracy in Pointing 
with Eyes Closed; Normal Reaction Movements in Response to Ves¬ 
tibular Irritation; Loss of Pointing Accuracy And Changes in Reac¬ 
tions to Vestibular Irritation in Cerebellar Disease. 394 

Cerebellar Centres, Function of. 394 

Effect—Disease or Destruction of. 394 

Location of. 395 

Evidences of Correct Localization. 395 

Normal Pointing Accuracy.. 395 

Method of Determining. 395 

Pointing Reactions in Response to Vestibular Disease. 395 

Method of Applying Tests. 395 

Changes in Pointing Accuracy in Cerebellar Disease. 396 

CHAPTER XV 

Surgical Operations for the Relief of Suppurative Lesions of the Middle 
Ear and Mastoid Process; Myringotomy; Mastoidectomy; The Radi¬ 
cal Operation; Ossiculectomy. 399 

Myringotomy; Incision of the Drum Membrane Paracentesis. 399 

Operative Dangers. 400 

Preparation for Operation. 402 

Anaesthesia. 403 

Technic. 403 

Possible Repetitions.:. 406 

Surgical Landmarks of the Mastoid Cortex. 406 

Mastoidectomy; The Mastoid Operation; Sometimes Called “Schwartze’s 

Operation ”.’. 409 

Preparation of the Patient. 409 

Instruments. 412 

Position of patient on Table. 412 

The Initial Incision. 413 

The Bone Operation. 414 

RationalThoroughness in Obliterating the Mastoid Cells .... 422 

The Element of Time in Mastoid Surgery". 425 

Postoperative Treatment. 425 

The “Blood-clot Operation” (Blake, Reik). 430 

Surgical Treatment of Chronic Middle-ear Suppuration. 432 

Radical Mastoid Operation; Schwarzte-Stacke Operation. 432 

Preparation of the Patient. 433 

The Incision. 433 

Facial Paralysis. 442 

Zanfal-Heine Operation. 443 

Stacke’s Operation ... 444 

The Korner Flap. 449 

The Panse Operation. 450 

The Siebenmann Flap. 450 

Postoperative Treatment.•. 451 

The Influence of the Radical Operation upon Hearing. 455 

The Heath Operation for Chronic Middle-ear Suppuration ... 455 

Bondy’s Operation. 456 

Streit’s Operation. 457 

Ossiculectomy. 457 

Preparation. 457 

The Instruments. 458 

Operation. 458 

Plastic Operations for Closing a Post auricular Opening Follow¬ 
ing the Radical Operation. 459 

Mosetig-Moorhof Operation. 459 

The Passau-Trautmann Operation. 460 

Author’s Operation for Preventing or Closing Postauricular 
Fistula Following the Radical Operation. 461 




















































XIV 


CONTENTS 


CHAPTER XVI 

LabYRINTHECTOMY; THE RADICAL LABYRINTH OPERATION; SURGICAL DRAINAGE OF 

the Labyrinth. 463 

Indications. 463 

Surgical Guides to the Vestibule. 404 

Operation. 465 

The Jansen Operation. 465 

Hinsberg’s Operation. 466 

Richards’s Operation. 467 

Neumann’s Operation. 468 

Comparative Advantages and Disadvantages of the Different 

Operations. 470 

Author’s Method of Reaching the Vestibule. .. 4/0 

Obliteration of the Vestibule for the Relief of Vertigo (Lake). 475 


CHAPTER XVII 


Surgical Treatment of Infective Sigmoid Sinus Thrombosis. 477 

Sinus Operation for the Removal of an Infected Clot. 479 

Use of the Rongeur. 481 

Exploration of the Sinus. ; . 483 

Resection of the Jugular Vein. 485 

Ligation of the Jugular Vein. 488 


CHAPTER XVIII 

Surgical Treatment of Intracranial Lesions (Continued): Temporo- 


SPHENOIDAL AND CEREBELLAR AbSCESSJ OTITIC MENINGITIS . 490 

Surgical Treatment of Brain Abscess. 490 

Cerebellar Abscess. 502 

Meningitis. 504 

Serous Meningitis. 504 

Serous Meningo-encephalitis (Korner). 506 

Purulent Leptomeningitis. 506 


CHAPTER XIX 


Facial Paralysis. 508 

Facial Paralysis of Otitic Origin. 508 

Postoperative Facial Paralysis. 508 

Symptoms and Physical Signs. 509 

Prognosis. 510 

Treatment. 510 


CHAPTER XX 


Congenital Abnormalities of the Auricle. 514 

Macrotia. 514 

Polyotia. 514 

Supernumerary Parts. 514 

Projecting Auricle, “Lop Ear” . 516 

Microtia. 516 

Treatment. 516 

Removal of Supernumerary Nodules. 521 

Treatment of Prominent or Projecting Ears. 521 

CHAPTER XXI 

Non-Suppurative Diseases of the Labyrinth. 526 

Meniere’s Disease. 526 

Etiology. 526 

Diagnosis. 526 

Symptoms.*.. 527 

Prognosis. 527 

Treatment. 527 
















































CONTENTS 


xv 


“Vertigo ab aure l^eso”. 528 

Leukemic Deafness. 528 

Symptoms. 529 

Anaemia of the Labyrinth. 529 

Treatment. 530 

Syphilis of the Labyrinth.. 530 

Treatment.. 532 

Tuberculosis of the Ear. 532 

Pathology. 533 

Symptoms. 534 

Diagnosis. .535 

Terminations. 535 

Prognosis. 536 

Treatment. 537 

CHAPTER XXII 

Otologic Lessons of the World War. War Deafness: Deafness Due to Di¬ 
rect Labyrinthine Injury : Concussion Deafness : Psychic Deafness . 
Pithiatism: Simulation: Pjthiatic Deafness: Diagnosis and Ra¬ 
tionale of Treatment. 538 

Deafness Due to Direct Cranial Injuries. 539 

Concussion Deafness Due to Explosions. 541 

Immunity of Static Labyrinth to Injury by Explosive Sounds. 542 

Prognosis as to Functional Improvement in Concussion Deafness. ..... 542 
Chief Differential Point Between Profound Deafness Due to Direct 
Labyrinthine Injury and to Concussion. 542 

Hysterical or Psychic Deafness; Psychic Mutism. 543 

Pithiatism, its Etiology and Clinical Significance ... 543 

Types of Pithiatic Deafness. 544 

Useful Diagnostic Tests. 545 

Rationale of Treatment. 545 

CHAPTER XXIII 

Salvarsan in the Treatment of Aural Disease. Auditory Nerve Lesions 

Occasionally Following Its Use. 548 

Cranial-nerve Lesions Following the Use of Salvarsan. 549 

CHAPTER XXIV 

Vaccine Therapy in the Treatment of Aural Disease : Autogenous Vaccines : 

Bactericidal Sera; Stock Vaccines. 554 

Preliminary Remarks. 554 

CHAPTER XXV 

Aural Disturbance Due to Dental Lesions. 558 

CHAPTER XXVI 

Deaf-mutism. 561 

Etiology.’. 561 

Morbid Anatomy. 564 

Treatment.. 565 

CHAPTER XXVII 

Nasopharyngeal Adenoids. 566 

Diagnosis.a. 566 

Treatment. 567 

CHAPTER XXVIII 

Tumors of the Eighth Nerve. 571 

Etiology—Pathology—Mechanical Influence on Adjacent Structures 572 








































XVI 


CONTENTS 


Symptoms: Gradually Developing Symptom-complex. 572 

Differential Diagnosis. 585 

Treatment: Choice of Surgical Methods. 584 

Diagnosis, With and Without Surgical Intervention. 584 

The Otologist’s Problem and Responsibilities. 583 

APPENDIX 

Aural Disease in Relation to Life Insurance.. 587 

Artificial Aids to Hearing. 588 

Case Histories. 589 

Formulae. 592 

Alkaline and antiseptic Solutions for Cleansing the Nasal and 

Nasopharyngeal Spaces. 592 

Oil Solutions.. . . .. 592 

Astringent and Antiseptic Solutions for Direct Application to the 

Pharyngeal Mouth of the Eustachian Tube. 593 

Ointments. 593 

Solution for Instillation into the Ears. 594 

Local Anaesthesia for Operation of Myringotomy. 594 

For the Relief of Moderate Pain. 595 

For the Relief of Nasopharyngeal and Tubal Congestion. 595 

Index. 597 



















ILLUSTRATIONS 


v. 

VI. 


COLOR PLATES p , 

PAGE 

Fig. 84. Lupus Hypertrophicus Auriculae. 104 

Fig. 85. Herpetic Eruption due to Inflammation of the Geniculate Ganglion.. 106 


CHARTS 


Chart No. 1. For Bedside Histories. 572 

Chart No. 2. For Office Histories. 573 


fig. ILLUSTRATIONS IN TEXT 

1. The Auricle. 

2. Auricular Cartilage. 

3. The Auricular Muscles., . v . 

4. Auriculo-meatal Cartilage. 

5. Petromastoid. 

6. Squamozygomatic, Outer Surface. 

7. Right Tympanic Ring.. 

8. Squamozygomatic, Inner Surface. 

9. Temporal Bone..V. 

10. Infant Skull. 

11. Infant Temporal Bone... 

12. Adult Temporal Bone. 

13. Diagram: Dotted Lines Showing Influence upon Direction of Canal of Draw¬ 

ing Auricle Upward and Backward.\.. 

14. Vertical Section through Tympanic Cavity and Bony Meatus. 

15. Inner Tympanic Wall. 

16. Tympanic Roof. 

17. Vertical Section of Temporal Bone, Showing Anterior Wall of Tympanum. . . 

18. Section Showing Posterior Wall of Tympanum... 

19. Horizontal Section through Tympanum, Showing Tympanic Floor. 

20. Inner, or Tympanic, View of Drum Membrane... 

21. Ossicles, Right and Left, Only Slightly Enlarged above Actual Size. 

22. Malleus, Enlarged. 

23. Incus. . . 

24. Stapes... 

25. Ossicles in Articulation. 

26. Diagrammatic Picture of the Membrana Tympani and Its Attachments .... 

27. Temporal Bone with Drum Membrane and Outer Wall of Vault Removed.. . 

28. Tympanum of Infant Six Months Old. (Left.). 

29. Tympanum of Infant Six Months Old. (Right.). 

30. Transverse Section of Eustachian Tube. 

31. Temporal Bone, Outer Surface. 

32. Temporal Bone, Inner Surface. 

33. Vertical Section of Temporal Bone Passing Through Aditus ad Antrum. 

34. Section through Mastoid Process of Pneumatic Variety. 

35. Section through Mastoid Process of Diploic Type. 

36. Section through Mastoid Process of Sclerotic Variety. 

37. Tuning-fork. 

38 and 39. Head Mirrors. 

40. Head-band and Mirror. 

41. Fibre Head-band. . 

42. Aural Specula.. 

43. Aural Forceps. 

44. Tympanic Probe. 

45. Aural Cotton Applicator. 


3 

3 

4 

5 
5 
5 
5 
5 
5 
7 
7 

9 

10 

11 

12 

13 

14 

15 
15 
17 
17 
17 
17 
17 
19 
21 
24 
24 
29 
33 
33 
33 
33 
33 
33 
35 

45 

46 

47 

48 
48 
48 
48 


XVII 














































xviii ILLUSTRATIONS 

46. Wall Bracket for Movable Electric Light. 49 

47. Forehead Lamp for Bedside Examination. 50 

48. Position of Physician and Patient for Aural Examination. 51 

49. Section through Adult Canal and Tympanum. 52 

50. Section through Canal and Tympanum of Infant at Term. 52 

51. Diagram Showing Direction of Auditory Canal of Adult. 52 

52. Diagram Showing Direction of Auditory Canal of Infant. 52 

53. Normal Drum Membrane. 54 

54. Diagram Showing Quadrants of Membrana Tensa. 55 

55. Semidiagrammatic Picture, Showing Relations of Ossicles in Vault and Atrium. 56 

56. Bulging Drum Membrane. 57 

57. Retracted Drum Membrane. 57 

58. Rough Pen-and-ink Diagram of the Drum Membrane. 58 

59. Siegel’s Otoscope. 59 

60. Politzer’s Inflating Apparatus. 61 

61. Eustachian Catheter. 62 

62. Dench Inflating Apparatus. 64 

63. Diagnostic Tube._. 64 

64. Position of Physician and Patient during Catheter Inflation... 66 

65. Correct Pathway of Catheter to Posterior Pharyngeal Wall. 68 

66 . Correct Position of Catheter within Tubal Orifice. 68 

67. Incorrect Introduction of Catheter. 68 

68 . Tongue Depressor (A). 68 

69. Nasal Speculum (B). 68 

70. Nasal Speculum (C). 68 

71. Laryngeal Mirror (D). 68 

72. Cotton Applicator (E). 68 

73. Nasal Probe (F).. . . 68 

74. Politzer’s Acoumeter. 74 

75. Hartmann’s Tuning-forks. 84 

76. Large Tuning-fork. 85 

77. Kerrison’s Set of Tuning-forks. 88 

78. Galton Whistle. 88 

79. Barany’s Noise Apparatus. 93 

80. Auricular Perichondritis. 102 

81. Deformity Resulting from Neglect of Lesion Shown in Fig. 80. 102 

82. Haematoma Auris, Resulting from Blow upon the Ear.103 

83. Final Permanent Deformity Resulting from Haematoma Auris. 104 

84. Lupus Hypertrophicus Auriculae. 104 

85. Herpetic Eruption due to Inflammation of the Geniculate Ganglion. 106 

86 . Displacement of Left Auricle. 110 

87. Necrosis of Auricular Cartilage and Deformity Resulting from Extension of 

Infection from a Furuncle in the Canal. 110 

88 . Furuncle Knife. 113 

89. Hyphomycetes, Moulds. 116 

90. Aural Syringe. 119 

91-93. Instruments for Removing Solid Substances from the Ear. 121 

94-96. Retracted Drum Membranes. 148 

97. Tubo-tympanic Congestion. 149 

98. Eustachian Cotton Applicator. 152 

99. Skull of Infant at Term. 154 

100. Skull of Adult. I 54 

101-103. Acute Catarrhal Otitis Media, First, Second and Third Stages. 163 

104. Diagrammatic Picture of Membranous Partitions of Vault. 166 

105-108. Acute Purulent Otitis Media, Four Successive Stages. 168 

109. Incision of Membrana Tensa. 174 

110 . Incision Indicated in Acute Purulent Otitis Media. 179 

111 . Incision through Drum-head and Posterosuperior Canal Wall. 179 

112 . Auricular Displacement Resulting from Postauricular Subperiosteal Abscess.. 186 

113. Aural Ice-bag. 189 

114. Leiter’s Coil. 189 

115. Bone Absorption Resulting from Cholesteatoma. 197 

116-124. Central Perforations. 201 

125-128. Marginal Perforations. 20 $ 































































ILLUSTRATIONS 


xix 


129-131. Perforations of Shrapnell’s Membrane. 

132. Yankauer’s Eustachian Curette. 

133. Aural Polyp. 

134-137. Perforations of Long Standing... 

138. Thickening Due to Calcareous Deposits.... 

139. Celluloid Bougies... 

140. Eustachian Catheter and Bougie... 

141. Eustachian Applicator. 

142. Yankauer’s Eustachian Applicator. 

143. Horizontal Section through Oval Window (Right),'Dividing Stapedial Foot¬ 

plate, Vestibule, and Basal Turn of Cochlea. 

144. Horizontal Section through Stapes and Basal Turn of Cochlea.. . !. 

145. Horizontal Section through Right Oval Window. 

146. Diagrams Showing Line of Incision, and the Resulting Flap, Deflected 

147. Bony Capsule of Labyrinth. 

148. Drawn from Metal Cast of Labyrinthine Cavity.. 

149. Horizontal Section through Internal Auditory Meatus, Cochlea, and Vestibule. 

150. Horizontal Sections through Modiolus from Base to Apex. 

151. Vertical Section through Tympanum, Vestibule, and Internal Auditory Meatus 

152. Labyrinthine Vestibule, with Roof Removed. 

153. Relative Positions of Three Semicircular Canals. 

154. Membranous Labyrinth. 

155. Diagrammatic Section of Ampullar End of Horizontal Semicircular Canal 

Showing Position of Crista Acustica. 

156. Structures Common to the Cristse Acusticse and Maculae Acusticae.’ . . i . 

157. Diagrammatic Cross-section of Cochlear Canal. 

158. Organ of Corti.,x. 

159. Inner and Outer Rods of Corti. 

160. Semicircular Canals of Pigeon. 

161. Diagrammatic Picture of Inner Tympanic Wall. 

162-166. Types of Vestibular Nystagmus. 

167. Revolving Chair: Patient and Physician in Position for Rotation Test. 

168-169. Author’s Scheme for Remembering Semicircular Canal Planes. 

170-172. Author’s Scheme for Remembering Exact Relative Positions of the Three 

Canals... 

173. Diagrammatic Picture of a Horizontal Section of Skull, Passing through 

Horizontal Semicircular Canal?. 

174-177. Diagrams Showing Falling Directions in Relation to Vestibular Nystagmus 

178. Diagrams Showing Different Forms of Rotation Nystagmus. 

179. Barany’s Fixator and Self-retaining Basin. 

180. Horizontal Section of Skull Passing through both Horizontal Semicircular 

Canals. Nystagmus During Rotation to Right. 

181. Nystagmus During Rotation to Left. 

182. After-nystagmus (i.e., Immediately Following Rotation to Right), Both Laby¬ 

rinths being Sound... 

183. After-nystagmus (i.e., Immediately Following Rotation to Left), Both Laby¬ 

rinths being Sound. 

184. After-nystagmus (i.e., Immediately Following Rotation to Right), Right Mem¬ 

branous Canal having been Destroyed by Disease. 

185. After-nystagmus (i.e.. Immediately Following Rotation to Left), Right Mem¬ 

branous Canal having been Destroyed by Disease. 

186. Diagrammatic Picture of a Transverse Section of the Brain. 

187. Chart Showing Important Aphasia Centres. 

188. Otitic Pathways of Pus to Brain or Meninges (Diagrammatic). 

189. Semi-diagrammatic Picture Showing Section of Sigmoid Sinus and Separation 

of Dural Layers... 

190. Showing Perisinous Abscess. 

191. Showing Possible Pathways of Infection... 

192. Venous Channels of the Brain. 

193. Invasion of Brain through Tympanic Vault. 

194. Vertical Cross Section of Brain Showing Influence of Transmitted Pressure 

from Temporosphenoidal Abscess upon Motor Area Above (Diagrammatic) 

195. Vertical Cross Section of Brain, Showing a Large Temporosphenoidal Abscess 

(Diagrammatic) .. 


203 

209 

210 
213 
227 

231 

232 

239 

240 

247 

248 

249 

259 

260 
260 
261 
262 

263 

264 

265 

266 


267 

268 
269 
271 
271 
278 
281 
2S2 

284 

285 


286 


287 

290 

291 

301 

302 
302 

302 

302 

302 

302 

329 

332 

337 

341 

341 

341 

356 

362 

369 


370 


















































XX 


ILLUSTRATIONS 


195a Vertical Cross Section of Brain, Showing Small Abscess Involving Internal 

Capsule (Diagrammatic). 

196. Inferior Surface of Encephalon. .... 

197. Incision Indicated in a Suppurative Lesion Confined to the Atrium. 

198. Incision Indicated in a Suppurative Lesion Involving the Tympanic Vault. 

199. Incision Supplementing Inadequate Perforation.... 

200. Incision Occasionally Indicated in Chronic Suppurative Otitis Media for the 

Evacuation of Pus Retained in the Vault.. # . 

201. Vertical Section through External Auditory Canal and Tympanic Cavity. 

202. Diagram Showing Technical Error Likely to Result from an Incision made 

from Above Downward.. 

203. Diagram Showing Double Movement (i.e., Downward and Inward) Required 

in Incising the Membrane from Above Downward._• 

204. Dangerous Accident (Stapedial Dislocation) which May Result from an Inci¬ 

sion from Above Downward.. 

205. Incision of Drum Membrane from Below Upward, the Correct Method. 

206. Correct Method of Holding Myringotome. 

207. Surgical Landmarks of Mastoid Cortex. 

208. Level of Safety in Opening Mastoid. 

209. Area Shaved for Mastoid Operation. 

210 . Instruments Called for in any Surgical Operation. 

211. Self-retaining Retractors.*. 

212. Langenbeck’s Periosteal Elevator. 

213. Large Grooved Chisel, or Gouge (A). 

214. Whiting’s Gouge (B).. 

215. Whiting’s Gouge (C).'. 

216. Jansen’s Chisel (D). 

217. Jansen’s Chisel (E)...:. 

218. Mastoid Mallet (F). 

219. Mastoid Rongeurs. 

220. Mastoid Curettes. 

221. Richards’s Mastoid Curettes.. 

222 . Wooden Head-rest, or Block, for Use in Mastoid Surgery.'. 

223. Initial Incisions for Exposing the Mastoid Cortex. 

224. Mastoid Cortex Adequately Exposed for Operation. 

225. Position of Gouge in Removing Mastoid Cortex. 

226. Representing the Extent and Outline of the Initial Opening Usually Made with 

the Mallet and Gouge. 

227. Illustrating the Use of the Rongeur in Removing the Mastoid Cortex. 

228. Diagram Showing the Use of the Bent Probe in Locating the Aditus. 

229. Lines Representing Surgical Guides to a Very Small Antrum. 

230. Vertical Section through the Aditus. 

231. Mastoid Excavation Completed, Showing Extensive Development of Zygo¬ 

matic Cells. 


370 

398 

399 
399 
399 

399 

401 

401 

401 

402 
402 
404 

407 

408 

409 

408 

409 
409 
408 
408 
408 
408 
408 

408 

409 

410 

411 

412 

413 

415 

416 

416 

417 

418 

419 

420 

421 


232. Line of Section Extending through Mastoid Process and Petrous Portion of 

the Temporal Bone. 422 

233. Pneumatic Spaces Extending from Mastoid Process to Apex of Petrous Bone... 423 

234. Continuous Chains of Pneumatic Spaces Extending from Mastoid to Petrous 

Portion of the Bone. 423 

235. Iodoform Gauze Plugs for Control of Hemorrhage in Case of Accidental Open¬ 

ing of Sinus. 425 

236. Operation of Mastoidectomy Completed. 427 

237. Mastoid Bandage. 427 

238. Postauricular Incision for the Radical Operation. 433 

239-240. First Stages of Radical Operation.. 434 

241. Jansen’s Chisel. 435 

242. Radical Operation. 435 

243. Radical Operation, after Removal of “ Bridge formed by Posterosuperior 

, Canal Wall.. 437 

244. Radical Operation, after Lower Half of Posterior Canal Wall has been Reduced 

so as to Appear as a Direct Continuation of the Facial Ridge. 438 

245. Tympanic Floor. 439 

246. Ring Curette. 440 



















































ILLUSTRATIONS 


xxi 


247. Tympanic Structures Usually Exposed in Radical Operation. 441 

248. Stacke’s Operation. 444 

249. Stacke’s Protector.'. 445 

250. Kerrison’s Tympanic Rongeur. 446 

251-254. Diagrams Illustrating Plastic Operations Forming Part of Radical Operation 448 

255. Narrow-bladed Knife Required in the Plastic Work of the Radical Operation .. 449 

256. Instruments Essential in the Operation of Ossiculectomy. 455 

257. Incision Lines in Ossiculectomy. 458 

258-261. Mosetig-Moorhof Operation, Four Successive Steps. 459 

262-265. Successive Steps of the Passau-Trautmann Operation. 460 

266-268. Author’s Operation for Preventing or Closing Postauricular Opening Fol¬ 
lowing Radical Operation. 462 

269. Section through Tympanum, Aquaeductus Fallopii, and Ampullar Ends of Hori¬ 

zontal and Anterior Vertical Canals. 463 

270. Hinsberg’s Labyrinthine Operation. 466 

271. So-called “Solid Angle”. 467 

272. Vertical Section through Aditus and Vertical Portion of Facial Canal. 468 

273. Surgical Guides to Vestibule (Neumann’s Operation). 469 

274. Radical Operation Preliminary to Opening Labyrinth. 471 

275. Excavation Preliminary to Uncovering Vestibule..... 472 

276. Author’s Curette. 472 

277. Vestibule with Roof Removed. 472 

278. Horizontal Section through Cochlea. 474 

279. Bone Operation Preliminary to Exposure of Sigmoid Sinus. 480 

280. Position of Chisel in Uncovering the Sigmoid sinus. 480 

281-282. Rongeurs.. 481 

283. Exposure of Sinus Wall Preliminary to Its Exploration... 482 

284. Position of Gauze Plugs for Controlling Hemorrhage when Sinus is Opened.... 483 

285. Line of Incision for Jugular Resection. 486 

286. Internal Jugular Vein. 487 

287. Relations of Brain to Temporal Bone... 490 

288. Incision for Exposing Squama, Preliminary to an Exploratory Operation for 

Brain Abscess . . -. 493 

289. Dural Exposure Preliminary to Exploration of the Brain for Suspected Tem- 

porosphenoidal Abscess. 495 

290. Narrow-bladed Knife for Exploring the Brain. 496 

291-292. Drawings Made from a Section of the Brain, Showing Schematically the 

Advantages of Exploring the Brain through Separate Incisions of the Dura 
as Compared with Exploratory Punctures in Different Directions through 
a Single Dural Incision. 497 

293. Whiting’s Encephaloscope.. 500 

294. Gauze Wmk for Use in Brain Abscess. 501 

295. Chart Showing Directions and Depths of Exploratory Punctures of Cerebellum 503 

296. Exposure of Dura Covering Cerebellum. 504 

297. Exposure of Dura Covering Cerebellum. 505 

298. (Exposure of Facial and Hypoglossal Nerves. 512 

299. Lateral Implantation of Facial Segment into Hypoglossal Trunk. 512 

309. Anastomosis of Facial and Hypoglossal Nerves. 513 

301-303. Three Common Types of Macrotia. 515 

304. Supernumerary Cartilaginous Nodules. 515 

305. Supernumerary Nodules. 515 

305. Projecting Auricle;‘‘Lop Ear”. 51b 

307-308. Microtia... • ... • • .. 

309-311. Usual Method of Reducing an Abnormally Large Auricle.519 

312-315. Operation for Reducing Abnormally Wide Auricle. 520 

316-318. Operation for the Correction of Moderate Projection. 522 

319-323. Ruttin’s Operation for Projecting Auricles. o23 

324-328. Duel’s Operation for Projecting Ears.• • • • .. ^ 

329. Radiogram Showing Abscess at Roots of Two Incisor Teeth. . .5oJ 

330. Radiogram: Roots of a Bicuspid Tooth Projecting into Antruni of Highmore... 5o9 

331. Radiogram Showing Imperfect (Partial) Eruption of \\ isdom Tooth. 559 

332-333. Radiograms: IJnerupted and Abnormally Placed Teeth.. .. .. ... - 5o9 

334. Area of Tumor Showing (X 80) Characteristic Architecture of the Fibrous ^ 

Areas .. • 574 

335-336. Characteristic Architecture of Fibrous and Recticular Areas. 574 












































































' 













■ 







I 















DISEASES OF THE EAR 


CHAPTER I. 

ANATOMY AND PHYSIOLOGY OF THE SOUND-CONDUCTING 

APPARATUS. 

’Anatomically, the ear may be divided into three parts,—viz., the 
outer ear (auricle and external auditory meatus), the middle ear (tym¬ 
panum and structures contained therein), and the inner ear, or labyrinth. 
Physiologically, the organ of hearing must be regarded as consisting of 
two distinct mechanisms,—viz. (1) a sound-conducting apparatus, having 
to do solely with the conduction, or transmission, of sound waves; and 
(2) a perceptive mechanism, an organ specialized for the reception and 
analysis of sound waves, and their appreciation as sound. 

From the view-point of the otologist, the latter is much the more prac¬ 
tical and useful division, suggesting at once the necessary separation of all 
aural disorders into two main groups,—viz. (1) those which originate in, or 
involve chiefly, the labyrinth or end-organs of the auditory nerve (labyrin¬ 
thine diseases); and (2) those depending upon pathological changes in some 
portion of the conducting mechanism (diseases of the conducting apparatus). 

The conducting apparatus is composed of the following structures: 
the auricle and external auditory meatus; the drum membrane, and ossicu¬ 
lar chain with the muscles and ligaments attached thereto; the tympanic 
cavity in which the ossicles are suspended, and the Eustachian tube. 

The perceptive apparatus includes: the auditory nerve, its nuclei of 
origin, trunk, association fibres, cortical nuclei, its terminal fibres in the 
cochlea, and the membranous cochlea itself. 

The Auricle, or Pinna (Fig. 1).—The auricle is an irregularly ovoid 
structure which might well be described as an outer terminal expansion 
of the cartilaginous meatus. It is roughly convex posteriorly, concave 
anteriorly. It consists chiefly of a thin cartilaginous plate, covered by 
perichondrium, to which the integument is closely adherent. The lower 
dependent portion, containing no cartilage, is composed of connective 
tissue containing some fat cells, and is called the lobule, or lobe of the ear 
(Fig. 1, 10). The free margin of the cartilaginous plate is curled toward 
the anterior surface of the auricle, forming a narrow ridge which is called 
the helix (1). The helix begins in front just above the orifice of the meatus, 
and ends behind at a point which marks the beginning of the posterior 
border of the lobule. Separated from the helix by a narrow curvilinear de¬ 
pression (the fossa of the helix, 2), and parallel with its posterior portion, 
is another elevation, known as the antihelix (4). The antihelix divides 
above into two arms, or crura, which inclose a triangular depression, the 

1 



2 


ANATOMY AND PHYSIOLOGY 


fossa of the antihelix (3). The antihelix terminates below in a prominence 
directed forward and upward, called the antitragus (8). Opposite this, 
but directed backward and somewhat overlapping the orifice of the meatus, 
is another projecting lamella of cartilage, the tragus (7). The tragus and 
antitragus are separated below by a deep notch, the incisura intertragica 
(9). These structures—viz., the antihelix above and behind, the anti¬ 
tragus and incisura intertragica below, and the tragus in front—form the 
boundaries of a deep central depression, the concha (5). In the anterior 
part of the floor of this concavity is the orifice of the external auditory 
canal (6). 

Helix (?) 

Fossa of the helix (2) 

Fossa of the antihelix (S) 
Antihelix («) 

Concha (5) 

Orifice of external auditory 

meatus (6) 

Tragus (?) 

Antitragus (8) 

Incisura intertragica (5) 

Lobule of the ear (10 


Fig. 1 . —The auricle. 



The auricle varies greatly in size and shape, and also in the angle 
which its posterior surface forms with the side of the skull. Its cartilagi¬ 
nous frame consists of a single plate of reticulated cartilage, the various 
folds of which assist in the formation of the elevations and depressions 
described above (Fig. 2). 

Muscles of the Auricle. —These consist of two sets,—viz. (A) those 
which arise from the side of the head and are inserted into some portion 
of the auricle, their contraction serving to move the auricle as a whole; 
and (B) those which have both origin and insertion upon the auricle itself, 
their contraction serving to change its form or shape. 

(A) The muscles arising from the side of the head are three in number, 
—viz., the attrahens aurem, or auricularis anterior; the attolens aure?n, or 
auricularis superior, and the retrahens aurem, or auricularis posterior. 
While man in the process of evolution has lost the voluntary control of 
these muscles, there are some partial exceptions to this rule, certain indi¬ 
viduals being able to move the ear in one or more directions (see Fig. 3). 




















MUSCLES OF AIJKICLE 


3 


(B) The second group of muscles—those having no attachment other 
than to the auricle itself—are six in number. Four of these—the helicis 
major, helicis minor, tragicus, and antitragicus—are attached to the an¬ 
terior, concave surface of the auricle, the other two—the transversus 



Fig. 2.—Auricular cartilage (from dissection by the author). 


auriculae and obliquus auris—being confined to its posterior surface. 
With the exception of the transversus auriculae and the obliquus auris, 
the form and distribution of all these muscles are clearly shown in the 
accompanying illustration (Fig. 3). 


Auricularis superior (attolens aurem) 



Auricularis posterior 
(retrahens aurem) 


The External Auditory Meatus. —The external canal in the adult 
consists of two parts,—(1) a membrano-cartilaginous tube, and (2) an 
inner bony tube, to which the former is joined. 


















4 


ANATOMY AND PHYSIOLOGY 



The membrano-cartilaginous canal (Fig. 4) is an inward tabular exten¬ 
sion of the auricle. Its external orifice is just behind the tragus in the 
anterior part of the floor of the concha. Its cartilaginous walls are deficient 
in the upper and posterior part of the canal, this deficiency being supplied 
by firm connective tissue which is continuous internally with the periosteal 
lining of the bony meatus. The cartilaginous frame of the meatus con¬ 
sists of an irregularly tongue-shaped plate of cartilage, curved longitu¬ 
dinally into a tortuous trough, which gives form to the outer half of the 

external canal. Its outer side, or base, which is 
continuous with the cartilaginous concha, is 
curved into an incomplete ring, deficient above 
and behind, which represents the orifice of the 
cartilaginous meatus. From this point its mar¬ 
gins gradually converge to form the narrow strip 
of cartilage the inner end of which is firmly at¬ 
tached to the rough outer extremity of the bony 
meatus. At the outer end of the canal, then, 
the anterior wall, floor, and part of the posterior 
wall are formed of cartilage; but as it extends 
inward, the cartilaginous plate becomes nar¬ 
rower until at its junction with the osseous 
meatus only the floor is formed of cartilage. 
The cartilaginous canal is rendered less rigid by 
two—sometimes three—fissures, passing through 
its anterior w r all. These fissures, more or less 
vertical in direction, and transverse to the long 
axis of the canal, are called the fissures of San¬ 
torini. They render the canal more pliable and lessen the amount of 
trauma in certain surgical operations requiring great displacement of the 
auricle. The general direction of the membrano-cartilaginous canal is 
inward and somewhat upward and backward. 

Development of the Osseous Meatus. —The external auditory canal 
presents marked differences in the adult and the infant at term. In order to 
obtain a clear view of the anatomy of the conducting apparatus, it is neces¬ 
sary to refer briefly to the development of the temporal bone, and trace cer¬ 
tain changes which it undergoes between birth and the middle of the fourth 
year, when it attains essentially the adult type. At birth the temporal 
bone is separable into three distinct parts,—the petromastoid, the squamo- 
zygomatic, and the tympanic. A fourth part, the styloid process, is carti¬ 
laginous at birth, and forms no part of the organ of hearing (see Plate I). 

In the primordial, or cartilaginous, skeleton there is but one repre¬ 
sentative of the future temporal bone,—viz., the so-called cartilaginous 
ear-capsule, which encloses the otic vesicle and its outgrowths (cochlea 
and semicircular canals), and therefore constitutes the essential part of 
the organ of hearing. This is later converted by numerous centres of 
ossification (Hertwig-Mark) into the os petrosum, or petromastoid. On 
the outer surface of the os petrosum (Plate I, 5) is an irregular depression 


Fig. 4.—Auriculo-meatal carti¬ 
lage, showing narrow strip of car¬ 
tilage entering into the formation 
of the membrano-cartilaginous 
meatus. 



DEVELOPMENT OP OSSEOUS MEATUS 


5 



Fig. 5. —Petromastoid: a, antrum; b, 
tegmen tympani; c, tympanic vault; d, 
incus; e, tympanic floor. 


Plate I. 



Fig. 6. — Squamozygomatic, 
outer surface: a, superior plate; b, 
Rivinian notch; c, inferior plate. 



Fig. 7.—Right 
tympanic ring, 
outer surface. 



Fig. 8. — Squamozygomatic, 
inner surface: a, inner horizontal 
plate (which forms part of the 
floor and the mid-cranial fossa); 
b, Rivinian notch. 



Fig. 9. —Temporal bone: a, squa¬ 
mozygomatic; b, tympanic ring; c, 
petromastoid bone, posterior half; 
d, inner tympanic wall; e, Rivinian 
notch. This figure shows the rela¬ 
tively enormous size of the infant 
tympanic cavity which is practically 
of the same size as in the adult. 



Fig. 10.—Infant skull, showing oblique position of the tympanic ring and drum membrane. 



















6 


ANATOMY AND PHYSIOLOGY 


or concavity, which represents the cavity of the middle ear, its bounda¬ 
ries constituting the inner wall, floor, roof, and also parts of the anterior 
and posterior walls of the tympanum. The tympanic cavity is completed 
by the squama and tympanic ring, which, with the drum membrane, 
form what in the adult becomes the outer tympanic wall. 

The tympanic ring and squamozygomatic portion of the temporal 
bone have no developmental relation to the cartilaginous cranium, being 
developed, each from a single centre of ossification (Heisler), from the 
connective tissue of its enveloping membrane. The tympanic ring (Plate 
I, 7) at birth is a small, somewhat flattened ring of bone, which is deficient 
in its upper and anterior eighth. Its inner concave margin presents a 
groove (sulcus tympanicus) for the attachment of the tympanic mem¬ 
brane, or membrana tensa. The tympanic ring is applied against the outer 
surface of the os petrosum, shutting in the lower and outer part of the 
infant middle-ear cavity. Firm osseous union occurs during the first year 
of life. The squamozygomatic (Plate I, 6) in the new-born infant is a 
flat plate of bone which externally is divided into two surfaces by the 
small zygomatic process. Above the zygoma is the shell-like lamina of 
bone which forms part of the outer wall of the mid-cranial fossa. Below 
the zygoma, the squama is formed of two plates, an outer and an inner. 
The outer plate, passing downward and somewhat inward from the level 
of the zygoma, forms the outer wall of the tympanic vault. Its lower 
border is concave, and, by articulation with the two extremities of the 
tympanic ring, completes the bony circle surrounding the drum membrane. 
The bony ring thus formed is of irregular outline. That part of it formed 
by the lower margin of the outer plate of the squama is ungrooved and does 
not give attachment to the membrana tensa, or drum membrane proper. 
It represents the arc of a small circle, and is known as the Rivinian segment 
(Plate I, 9, e). The tense membrane (membrana propria) is attached only 
to the grooved concave margin of the tympanic process and between its 
upper margin and the lower margin of the squama is a space known as the 
Rivinian notch (9, e). This space in the living subject is closed by the 
membrana flaccida, or ShrapneU’s membrane, to be described later. 

The inner, or horizontal, plate of the squama bends inward at about 
the level of the zygoma, and, by articulation with the tegmen tympani, 
enters into the formation of the floor of the middle fossa of the skull (8, a). 

The articulations of the bones which unite to form the infant temporal 
bone are clearly indicated by the illustrations of Plate I. Fig. 9 shows the 
temporal bone of an infant a few weeks old. It does not, however, cor¬ 
rectly indicate its position when in articulation with the other bones of 
the cranium. This is better shown by Fig. 10, in which the drum membrane 
is shown foreshortened by its very oblique position. In fact, so nearly do 
the tympanic ring and drum membrane approach the horizontal plane at 
birth that they seem to constitute the inferior, rather than the outer, wall 
of the tympanic cavity at this stage of tympanic development. 

The external auditory canal and drum membrane of the infant at term 
present the following differences from the adult type: (1) There is no bony 


DEVELOPMENT OF AUDITORY CANAL 


7 


meatus; the drum membrane is, therefore, not protected by its position 
at the fundus of a bony canal, but lies in the same plane as the outer 
inferior surface of the skull. Its position more nearly approaches the 
horizontal plane than in the adult. (2) The entire external canal is mem- 
brano-cartilaginous; its direction is outward and upward, so that the 
drum membrane and the roof of the meatus are nearly in the same plane. 
The floor of the canal is in contact with the roof. These facts have a 
practical bearing upon the examination of the ears of infants, it being 
necessary by downward traction of the lobe to draw the inferior wall 
away from the roof, and change the direction of the canal so that the 
drum membrane may be brought into view. 

Post-natal Changes. —Shortly after birth the following changes are 
inaugurated: By deposition of new bone upon the outer surface of the 
tympanic process or ring, this bone is converted into a bony trough, which 
forms the anterior wall, floor, and greater part of the posterior wall of the 
bony canal. That the conversion of the tympanic ring into a partial 
canal is effected solely by deposition of new bone upon its outer surface is 
evidenced by the position of the sulcus tympanicus, which remains un¬ 
changed,— i.e.j at the inner margin of the canal. Coincidently with these 
changes in the tympanic ring, the roof of the osseous meatus is formed by 



Fig. 11.—Infant temporal bone. Fig. 12.—Adult temporal bona 


the following changes in the squama: The outer plate is gradually bent 
inward at the level of the zygoma, thus forming an angle with the superior, 
parietal plate and finally in the adult bone assuming a position nearly, 
but not quite, horizontal. That the superior wall of the bony meatus 
results largely from this bending of the outer plate of the squama, rather 
than from massed deposition of bone at any particular point, is shown by 
the changed relation of the posterior root of the zygoma, which at birth 
is 5 to 6 mm. above the upper margin of the tympanic orifice, and in the 
adult marks the upper boundary of the bony meatus (Figs. 11 and 12, a). 




8 


ANATOMY AND PHYSIOLOGY 


These changes progress with remarkable rapidity, so that early in the 
second year of life the drum membrane is located at the fundus of a short, 
incomplete, but well-defined canal. Coincident with the development of 
the bony canal, changes quite as marked are taking place in the membrano- 
cartilaginous meatus. As the tympanic ring is built out into a bony 
trough, the anterior wall, floor, and posterior wall of the membranous 
meatus are drawn downward and outward, becoming adherent as a mem- 
brano-cutaneous lining to the walls of the osseous canal. The floor of the 
membranous meatus is, therefore, no longer in contact with the roof. At 
the end of the first year, the interior of the meatus in its natural position 
no longer presents the appearance of a transverse slit as at birth, but of a 
tube with a well-defined lumen. 

The Osseous Meatus. —In the adult the bony canal presents fairly 
constant characteristics. Its four walls— i.e., the superior, anterior, infe¬ 
rior, and posterior—differ in structure, conformation, and length. The 
superior wall, or roof, is formed of the outer plate of the squama, its 
direction from without being inward and slightly downward. The an¬ 
terior wall and floor are formed of very dense bone, and developed wholly 
from the tympanic ring. They are markedly convex in the direction of 
the long axis of the canal. The greatest convexity of both the anterior 
wall and floor is found at a point nearer the inner than the outer extremity 
of the canal. This is the narrowest part of the bony meatus and is called 
the isthmus. Beyond the isthmus, the floor dips strongly downward to the 
point of attachment of the inferior margin of the drum membrane, forming 
a depression, or sulcus, in which foreign bodies if small may be hidden from 
view. The posterior wall is composed in part of the dense tympanic plate, 
and partly of the premastoid plate from the outer lamella of the squama. 

A consideration of the relative length of the different walls of the canal 
helps one to appreciate the oblique position of the drum membrane. The 
anterior wall is longer and projects 5 or 6 mm. further inward than the 
posterior wall, and the floor projects further inward by 5 or 6 mm. than 
the roof. As the inner, terminal margins of these walls merge into the 
elliptical frame or groove which supports the drum membrane, it is obvious 
that the latter occupies a plane which forms an obtuse angle with the 
superior and posterior walls, and an acute angle with the anterior wall and 
floor. The drum membrane is, therefore, not placed vertically or at right 
angles to the long axis of the canal, its outer surface looking outward, 
downward, and forward. 

Politzer gives the average length of the four walls of the bony canal 
as follows: superior wall, 14 mm.; inferior wall, 16 mm.; posterior wall, 
15-16 mm.; and anterior wall 17-18 mm. Some years ago the author 
made careful measurements of a series of bones with a view of determin¬ 
ing the length of the postero-superior canal wall,— i.e., taken from the 
annulus tympanicus internally to the spine of Henle externally,—and 
found variations between 12 and 18 mm., the average being 14.5 mm. 
Obviously the length of the bony canal is subject to very considerable 


LENGTH OF AUDITORY CANAL 


9 


variations in different individuals. Cross section of the outer third of the 
bony meatus shows it to be of rather circular form, whereas internally— 
i.e., beyond the isthmus—it becomes elliptical. 

The external auditory canal as a whole presents great variations in 
different individuals. Some are wide and sufficiently straight to allow 
easy inspection of the drum mem¬ 
brane, while others are narrow and 
present curves necessitating con¬ 
siderable manipulation in order to 
bring the lower half of the drum 
membrane into view. The length 
varies from 1 to V /2 inches, 134 
inches being about the average. Of 
this the bony canal forms rather less 
than half. The membrano-carti- 
laginous portion is somewhat curled 
upon its long axis, and is rather 
wider in its central portion than at 
its orifice in the concha or at its 
junction with the bony meatus. 

The long axes of the two portions 
of the canal are not in the same 
straight line, the membrano-carti- 
laginous part being directed inward 
and slightly upward and backward, 
and the osseous canal inward and 
slightly downward and forward. It 
is often necessary, therefore, in order thoroughly to inspect the drum 
membrane, to draw the auricle upward and backward, thus bringing the 
two portions of the canal into the same straight line and the lower portion 
of the membrana tympani into view. 

The integument lining the auditory canal is continuous externally 
with that of the concha, and internally with that covering the outer sur¬ 
face of the drum membrane. The skin covering the drum membrane and 
canal seems to grow eccentrically from a point at the centre of the mem¬ 
brana tympani, light substances— e.g., small disks of paper—attached to 
any part of the drum membrane being found to travel first to its periphery 
and thence along the wall of the canal to the concha. The integument is 
much thicker in the membrano-cartilaginous than in the bony meatus. 
In the membranous canal it is from 1 to 13^2 mm. m thickness, and contains 
hair-follicles, sebaceous glands, and numerous ceruminous glands. The 
latter are arranged thickly in the posterior wall and floor. The ducts of 
the ceruminous glands may open either directly into the auditory canal 
or into the hair-follicles. 

The Tympanum.—The tympanum (tympanic or middle-ear cavity) 
is the name applied to the bony space which contains the ossicular chain. 


1 

1 



Fig. 13.—Diagram: dotted lines showing influ¬ 
ence upon direction of canal of drawing auricle 
upward and backward. 


10 


ANATOMY AND PHYSIOLOGY 


Its outer wall is composed largely of the drum membrane, and but for this 
structure it would be open to the outside air by way of the external audi¬ 
tory canal. It does communicate with the nasopharynx by means of the 
Eustachian tube. The roof of the tympanum lies on a plane considerably 
higher than the roof of the bony meatus, and its floor lies below the level 
of the floor of the bony canal. This fact has led to its being considered as 
composed of three parts,—namely: 

(1) The vault (attic, epitympanic space), or that portion of the tym¬ 
panic cavity lying above the level of the short process of the malleus. 

(2) The atrium, or that portion of the middle-ear cavity the upper 
and lower boundaries of which are horizontal lines, or planes, passing 
through the upper and lower margins of the membrana tensa. 

(3) The hypotympanic space, or that part lying below the level of the 
floor of the bony canal (Fig. 14), 



Fig. 14.—Vertical section through tympanic cavity and bony meatus. Above line A-B, tympanic 
vault. Between lines A-B and C-D, atrium. Below line C-D, hypotympanic space. 


The tympanum, or middle ear, viewed as a whole, is an irregularly 
wedge-shaped cavity, lying for the most part between the outer surface of 
the petrous bone and the drum membrane. Its greatest diameter is the 
vertical; its smallest is from without inward,— i.e., from the drum mem¬ 
brane to the inner tympanic wall. Its roof corresponds in position with 
the floor of the middle cerebral fossa; its floor is in relation with the jugular 

fossa which lodges the bulb of the jugular vein. The roof is much wider_ 

from without inward—than the floor, which measures but 2 to 3 mm. 
The gradual convergence from above downward of the outer and inner 














ANATOMY OF TYMPANUM 


11 


walls brings the cavity of the tympanum somewhat into the form of a 
wedge, the edge of which—directed downward and inward—corresponds 
with the tympanic floor. 

The tympanic cavity presents six walls, which call for careful study. 

The Inner Wall (Fig. 15).—The inner wall of the tympanum is 
formed by the outer surface of the petrous bone. It presents the following 
important landmarks: At a variable distance above the mid-point between 
the roof and floor is a well-marked ridge running from before backward 
(Fig. 15, a), and forming a natural boundary line between the inner wall 
of the vault and the inner wall of the atrium. This is formed by the outer 
wall of the Fallopian canal, which lodges the facial nerve. Just below the 
posterior half of the facial ridge is an oval depression, the fossa ovalis, at 
the bottom of which the oval window (Fig. 15, b) is plainly visible. The 
long diameter of the oval window is horizontal. It leads inward and 

Facial ridge (a) Oval window (6) 


Incomplete canal for tensor 
tympani muscle (/) 


Orifice of Eustachian canal (e) 

Round window (d) 

Fig. 15.—Inner tympanic wall (drum membrane and outer bony wall of tympanic vault removed). 



somewhat backward into the central cavity of the bony labyrinth (vesti¬ 
bule). In the living subject it is closed by the foot-plate of the stapes. 
Below the oval window the inner wall bulges into the cavity of the atrium, 
forming a rounded eminence, convex from above downward, called the 
promontory. This prominence is formed by part of the first turn of the 
cochlea. In form it resembles roughly the lateral half of a cone divided 
longitudinally from apex to base, the apex being directed forward and the 
base backward. Immediately behind the promontory, and below and some¬ 
what behind the oval window, is another depression, the niche of the round 
window (15, d). From this niche a somewhat circular orifice, the fenestra 
rotunda, leads forward and inward into that portion of the spiral tube of 
the cochlea known as the scala tympani. The round window is closed by 






12 


ANATOMY AND PHYSIOLOGY 


a delicate membrane which has received the name membrana tympani 
secundaria (Scarpa). Again comparing the promontory to a divided cone, 
we find that the apex is lost near the junction of the inner and anterior 
walls, or rather where the anterior wall merges into the funnel-shaped 
orifice of the Eustachian tube (e). Just above the Eustachian tube is the 
canal for the tensor tympani muscle. That portion of the tensor tympani 
canal presenting upon the inner wall of the tympanum is usually incom¬ 
plete (15, /). It passes obliquely upward and backward above the prom¬ 
ontory to a point in front of the anterior end of the oval window. Here it 
terminates in a thin lamella of bone, curled somewhat outward (processus 
cochleariformis), around which the tendon of the tensor tympani turns to 
pass outward and downward to its attachment to the hammer handle. 
Passing now to the vault, we find just above and parallel with the posterior 
end of the facial ridge a linear elevation of the inner wall. This elevation 
marks the position of the external or horizontal semicircular canal. It 
occurs not as a distinct ridge, but simply as a longitudinal bulging of the 
inner wall at this point (15, c). It is characterized chiefly by the smooth 
and ivory-like density of the bone in this situation. 

The Superior Wall (Fig. 16).—The roof of the tympanum is of 
surgical interest chiefly from the fact that its upper surface forms part of 



the floor of the middle cerebral fossa. It is of varying thickness in differ¬ 
ent bones, is often exceedingly thin, and occasionally exhibits defects of 
continuity (apertures), in which case the cavity of the middle ear is sepa¬ 
rated from the middle fossa of the skull only by loose connective tissue. 
The plate of bone forming the roof is a direct continuation of that covering 
the superior surface of the petrous bone. Externally it is united to the 








ANATOMY OF TYMPANUM 


' 13 

inner horizontal plate of the squama, forming the petrosquamosal suture, 
which is plainly visible in infancy and occasionally persists in adult life. 
A statement repeated in several text-books is to the effect that the inner 
horizontal plate of the squama enters into the formation of the tympanic 
roof. This statement is not correct. In any temporal bone in which the 
petrosquamosal suture can be recognized, it will be found that, if we make 
a vertical perforation downward through this suture, the instrument will 
appear below in the bony meatus and not in the tympanic cavity. The 
roof of the tympanum is formed, therefore, wholly by the superior plate of 
the os petrosum. 

The Anterior Wall (Fig. 17).—The upper and lower limits of the ante¬ 
rior wall of the tympanum are not clearly defined. Superiorly it merges 
by a gentle curve into the roof, and below it presents no angle of junction 
or natural landmark separating it from the tympanic floor. Internally 
and externally its limits are clearly defined by the inner and outer walls. 
It presents two prominent landmarks,—namely, the mouth of the Eusta¬ 
chian tube and the canal for the tensor tympani muscle. Two or three 



Fig. 17.—Vertical section of temporal bone, showing anterior wall of tympanum. 

mm. above the level of the tympanic floor is the tympanic orifice of the 
Eustachian tube (Fig. 17, a). The length of this bony canal averages 
about 12 mm. Its direction from the tympanum is forward, inward, and 
downward. Just above the Eustachian orifice is the beginning of the 
tympanic portion of the canal for the tensor tympani muscle (c), which has 
already been described in connection with the inner tympanic wall. This 
canal begins at the base of the skull in the anterior part of the petrous bone. 
In its passage through the petrous bone it lies just above and internal to 










14 


ANATOMY AND PHYSIOLOGY 


the Eustachian canal, from which it is separated by a thin lamella of bone. 
The lower portion of the anterior tympanic wall is in relation to the canal 
for the internal carotid artery. In this situation the bony plate separating 
the middle-ear cavity from the artery is in some bones exceedingly thin. 

The Posterior Wall (Fig. 18).—The posterior wall presents two 
portions which must be examined separately, — namely, the posterior 
wall of the vault and the posterior wall of the atrium. The posterior 
wall of the vault presents centrally a large, irregularly triangular opening 
the base of which is directed upward and the apex downward. This tri¬ 
angular opening is known as the aclitus ad antrum, and marks the divid¬ 
ing line between the tympanic vault and the so-called mastoid antrum. 



Tympanic fl 


Ampulla of horizontal 
semicircular canal 

Labyrinthine vestibule 


Internal auditory me 


Posterior wall of vault, 
showing aditus ad antrum 

Posterior wall of 
bony meatus 

Posterior wall of atrium 


Fig. 18. —Section showing posterior wall of tympanum. 


The antrum in reality is nothing more than a posterior prolongation of the 
vault. The posterior wall of the atrium is narrow from within out, its 
greater diameter being the vertical. Its chief landmark is a small pyra¬ 
midal process (processus pyramidalis) which projects forward into the 
atrium a little above the mid-point between the round and oval windows. 
It incloses a canal which contains the stapedius muscle, and presents 
at its apex a small opening through which the stapedius emerges to pass 
forward to its attachment to the neck of the stapes. 

The Inferior Wall (Fig. 19).—The floor of the tympanum is a nar¬ 
row space inclosed between the lower segment of the annulus tympanicus 
externally and the inner wall of the hypotympanic space internally. 
Viewed from above downward, it appears as a narrow depression, 5 to 7 
mm. long and 2 to 3 mm. wide, containing more or less cancellous or di¬ 
ploic tissue. This diploic tissue throws into clear relief the hard, compact 
bone of the floor of the osseous canal, which forms its outer boundary. 
The floor of the tympanum is in relation anteriorly with the canal for the 
internal carotid artery, posteriorly with the jugular fossa. The bony 
plates separating the hypotympanic space from the artery in front and 









ANATOMY OF TYMPANUM 


15 


the bulb of the jugular vein behind are sometimes exceedingly thin. More¬ 
over, cases have been observed in which, as a congenital defect or as a result 



Fig. 19.—Horizontal section through tympanum, showing tympanic floor. 

of necrosis, defects in the tympanic floor have allowed one or the other of 
these vessels to protrude into the lower part of the tympanic cavity,—a 
fact which, though exceedingly rare, should be borne in mind in carrying 
out any surgical measures in this region. 

The External Wall. —It now remains to be explained how this 
irregular but perfect little cavity is closed externally. The outer wall is 



Fig. 20.—Inner, or tympanic, view of drum membrane. 


formed chiefly by the membrana tympani,’ but, since the middle ear ex¬ 
tends in all directions somewhat beyond the limits of the drum membrane, 





16 


ANATOMY AND PHYSIOLOGY 


there is a peripheral frame of bone which mast be accounted for as part of 
the outer wall. This in the atrium and hypotympanic space consists of 
the inner surface of the tympanic ring. In the vault the outer wall is 
formed of the thickened inner edge of the outer inferior plate of the squama. 
This presents usually a fairly compact surface of bone (Fig. 20). 

The Annulus Tympanicus.—The inner margin of the bony meatus 
forms an irregular ring (annulus tympanicus), to which the drum mem¬ 
brane is attached. Owing to inequalities in the lengths of the different 
walls—the floor and anterior wall being longer and extending further 
inward than the roof and the posterior wall—this ring is irregularly ovoid 
or elliptical in shape, the long axis of the ellipse being from above down¬ 
ward and forward. These peculiarities also explain the oblique position 
of the drum membrane, which is not at right angles to the long axis of the 
bony meatus but forms decidedly obtuse angles with its roof and posterior 
wall. 

The Drum Membrane.—The membrana tympani is the strong lamina 
of fibrous tissue which forms the outer boundary of the middle ear. It 
is covered externally by integument continuous with that lining the ex¬ 
ternal auditory canal, internally by mucous membrane continuous with 
that covering the tympanic walls. Centrally it is drawn inward by the 
lower end of the hammer handle, to which it is attached, so that its outer 
surface is concave. It is attached peripherally to the concave margin of 
the annulus tympanicus, so that it necessarily assumes the oblique posi¬ 
tion of that bony ring, its outer surface looking outward and also strongly 
downward and forward. So intimately is it connected with certain parts 
of the malleus that it is impossible to give any practical description of the 
drum membrane without assuming some knowledge of the anatomical 
peculiarities of that little bone. We shall pause, therefore, in order to 
describe briefly the ossicular chain. 

The Ossicles.—The auditory ossicles are a system of little articulated 
bones, three in number, which connect the drum membrane with the 
labyrinth. The malleus, placed externally, is directly connected with the 
drum membrane; the stapes, the smallest of the three, presents a flat¬ 
tened bean-shaped surface which fits into and closes the oval window; 
and the incus, or middle bone, articulates externally with the malleus and 
internally with the stapes, thus forming a chain of movable levers which 
responds easily to the slightest movements of the drum membrane and 
transmits all sonorous impressions through the oval window to the laby¬ 
rinth and end-organs of the auditory nerve. 

The malleus, or hammer (Plate II, 22), is the only one of the ossicles 
which is in direct contact with the drum membrane, and is therefore the 
only one which can invariably be seen through the auditory canal. The 
head (22, A) is the upper, rounded portion which articulates with the body 
of the incus. It is smooth in all its aspects except the posterior, which 
presents an irregular surface for articulation with a rough depression on 
the anterior surface of the incus. It terminates below in a constricted 


THE AUDITORY OSSICLES 


17 



Fig. 21. —Ossicles, right and left, only slightly enlarged above actual size. 



22 23 24 25 

Fig. 22.—Malleus, enlarged; A, head; B, articular process; C, cog-process; D, neck; E, hammer 
handle; F, umbo, G, short process. 

Fig. 23.—Incus; A, body; B, short process; C, long arm; D, cog-process. 

Fig. 24.—Stapes; A, head; B, neck; C,C, crura; D, foot-plate. 

Fig. 25.—Ossicles in articulation; A, cog-processes in apposition; B, incudo-stapedial joint; C, 
foot-plate. 




18 


ANATOMY AND PHYSIOLOGY 


portion, the neck (22, D). Passing downward and backward from the 
neck is a narrow shaft of bone called the hammer handle, or manubrium 
mallei (E). The handle presents two rather sharp edges,—an external 
edge attached to the drum membrane, and an inner edge directed toward 
the inner tympanic wall. These two edges are separated by two compara¬ 
tively broad surfaces which are directed forward and backward respectively. 
At its lower extremity the hammer handle broadens into a somewhat 
flattened surface of bone called the umbo (F). At the beginning of the 
external margin of the hammer handle, or rather at its junction with the 
neck, is a short, pointed process of bone, directed outward and somewhat 
forward and upward, the short process (G). This also is in contact with 
the drum membrane, which it pushes before it into the cavity of the audi¬ 
tory canal. As viewed by reflected light through the auditory meatus, it 
appears as a small, whitish glistening projection in the upper anterior 
quadrant of the membrana tympani, and constitutes one of the most 
constant and useful landmarks. From the anterior surface of the neck, a 
slender spiculum of bone passes forward and slightly downward, its an¬ 
terior extremity lodging in the Glaserian fissure (see mallei in small figures, 
Plate II, 21). This is the long process of the malleus, or processus foli- 
anus. It is always present at birth, but is usually absorbed later in life. 
Its position is identical with that of the anterior ligament of the malleus, 
which usually surrounds it. 

The incus (Plate II, 23) is the central link of the ossicular chain. It 
consists of a body and two processes. The body (23, A) with the short 
process (B) forms an irregular cone, flattened from without inward, and 
presenting on its anterior surface, or base, a rough depression for articula¬ 
tion with the head of the malleus. Posteriorly the body terminates in a 
somewhat pointed extremity, the short process of the incus (23, B). Ex¬ 
tending downward from the anterior inferior corner of the body, and almost 
at right angles with its long axis, is a slender shaft of bone, the long arm 
(23, C). When the ossicles are in normal position, this process extends 
downward and backward, and is almost parallel with the manubrium 
mallei. Its lower extremity hooks sharply inward, and terminates in a 
rounded surface for articulation with the head of the stapes. This is 
known as the lenticular process. 

The stapes (Plate II, 24) is the smallest and—functionally at least— 
the most important of the three ossicles. It resembles almost perfectly a 
stirrup in form, and consists of a head (A), neck (B), two crura (C), and a 
bean-shaped plate of bone, the foot-plate (D), which fits into and closes the 
oval window. The foot-plate varies somewhat in size and shape in differ¬ 
ent individuals to conform to variations in the size and shape of the oval 
window. The arms, or crura, arise from either end of the outer surface 
of the foot-plate, and gradually converge to meet in a small button-shaped 
process, the head. Between the head and the point of junction of the two 
crura is a circular constriction, the neck. Upon the outer surface of the 
head is a very slight depression, or facet, which receives the lenticular 
2 


THE MEMBRANA TYMPANI 


19 


process of the incus. When the foot-plate is in its normal position within 
the oval window, the whole ossicle is somewhat depressed within the oval 
niche, the head extending but slightly into the cavity of the atrium. 

We are now in a better position to study the structural peculiarities 
of the membrana tympani, which the accompanying diagram may help 
to make clear. 

As stated in a foregoing paragraph, the drum membrane is composed 
of three layers,—an external cuticular, a middle fibrous, and an internal 
layer of mucous membrane. The outer, cuticular layer is easily separated 
from the underlying fibrous membrane, as is frequently shown by its 
early exfoliation when the drum membrane is the seat of an acute inflam¬ 
mation. The internal, mucous layer, on the other hand, is so closely 
adherent as to be practically inseparable. 

The drum membrane as a whole is divisible into two parts,—(1) the 
tense membrane, or membrana propria; and (2) the flaccid membrane, or 
Shrapnell’s membrane. 

The membrana tensa forms the outer wall of the atrium. It is attached 
peripherally to the sulcus tympanicus, or that portion of the annulus 
tympanicus which represents the original auditory process, or tympanic 
ring. Toward the upper and anterior pole of the drum membrane is seen 
in the living subject a small knob-like projection. This is the short process 
of the malleus (Fig. 26, D). Extending downward and backward from 



Annulus tympanicus (T) 
Circular fibres ( H ) 


Posterior attachment stria of Prussak ( A) 


Posterior extremity of 
tympanic ring ( L ) 

Posterior fold of membrana 
tympani ( K) 


Shrapnell’s membrane, inclosing the 
Rivinian notch, also spoken of as 
Prussak’s space ( B ) 


Rivinian segment (CO 

Anterior extremity of 
tympanic ring (L) 

Anterior attachment stria 
of Prussak (A) 

Short process (D) 

Hammer handle ( E ) 


Radiating fibres ( J ) 


Umbo (F) 


Fig. 26.—Diagrammatic picture of the membrana tympani and its attachments. 


the short process to the centre of the drum membrane is a line showing the 
position of the hammer handle (26, E), the lower terminal expansion of 
which is known as the umbo (F). The middle fibrous layer of the drum 
membrane is confined to the membrana tensa. It is composed of two 
layers,—an outer layer of radiating fibres (G, J), and an inner layer of 
circular fibres (H). The outer, radiating fibres are attached centrally to 
















20 


ANATOMY AND PHYSIOLOGY 


the umbo and to some extent also to the lower half of the hammer handle, 
from which central attachment they radiate toward the periphery of the 
membrane. They are therefore more closely arranged at the centre, and 
for this reason appear thicker and more numerous here than at the peri¬ 
phery. The inner circular fibres are arranged in concentric circles about 
the umbo. They are very sparsely distributed toward the centre of the 
membrane, but are much more numerous in the outer circles. In the upper 
part of the membrane they cross the radiating fibres in considerable 
numbers. The circular fibres are said to collect at the periphery and, 
together with certain cartilage-cells and tough connective-tissue fibres, 
aid in forming the thickened peripheral margin (annulus tendinosus) 
which is inserted into the tympanic ring. 

The membrana propria (M. tensa) is inserted into the tympanic groove 
throughout the entire extent of the original tympanic ring. Between the 
anterior and posterior extremities of the tympanic ring (spina tympanica 
major and spina tympanica minor), the upper margin of the membrana 
tensa has no bony attachment except to the short process of the malleus. 
In the living subject this upper margin is sometimes indicated by two 
delicate lines radiating from the short process, one leading forward to the 
spina tympanica major and the other leading upward and backward to 
the spina tympanica minor. These two lines (A, A) are known as the 
attachment striae of Prussak. Between Prussak’s striae below and the 
Rivinian segment above, is a small, somewhat fan-shaped space known as 
the Rivinian notch (B). This space is inclosed by the membrana flaccida 
(Shrapnell’s membrane), next to be described. Below the posterior stria 
of Prussak, and more horizontal in direction, is a prominent fold of the 
drum membrane, always easily discernible, known as the posterior fold 
(K). It passes backward from the short process to the tympanic ring. 

Shrapnell’s Membrane.—The Rivinian space, or notch, is closed by 
a membrane which is thinner and less tense than the membrana tensa; 
hence the name, membrana flaccida. It consists chiefly of an outer cuta¬ 
neous layer continuous with the integument covering the membrana 
tensa and the roof of the bony meatus, and an inner layer of mucous 
membrane continuous with that lining the tympanic cavity. Between 
these there are a few interlacing fibres of delicate connective tissue, but 
there is no distinct layer of fibrous tissue. It is in reality a very small 
membrane which is sometimes difficult to outline in the living subject: 
that is to say, there sometimes seems to be no demonstrable space between 
the strise of Prussak and the inner margin of the roof of the bony meatus 
(incisura Rivini). Shrapnell’s membrane forms part of the outer wall of 
the vault, and measures, according to Politzer, 1 }A mm. vertically and 
2 mm. transversely,— i.e., from before backward. 

The Ossicles, their Articulations and Relative Positions within the 
Tympanum (Fig. 27). — Before going further it is essential that the 
student should have a clear understanding of the position within the 
middle ear of the different parts of the ossicular chain. 


THE OSSICULAR CHAIN 


21 


The ossicles are lodged partly in the vault and partly in the atrium. 
In the vault are found the head of the malleus and the body of the incus. 
The remaining parts of the ossicular chain— i.e., the short process and 
handle of the malleus, the long arm of the incus, and the stapes—are 
located within the atrium. 

The Malleus. —The head of the malleus is lodged in the anterior 
part of the vault. Posteriorly it presents a rough surface for articulation 
with the incus. The neck of the malleus is on a level slightly below the 
inner margin of the roof of the bony meatus. Just below the outer ante- 


Short process of incus 


Head of malleus 



Fig. 27.—Temporal bone with drum membrane and outer wall of vault removed, showing relative 

position and ligaments of the ossicles. 


rior surface of the neck, the short process projects into the cavity, or lumen, 
of the bony canal, pushing the drum membrane before it. An imaginary 
horizontal line tangent to the upper surface of the short process (Fig. 27, 
AB) marks the boundary line between the atrium and vault. Extending 
downward and backward from the short process is the hammer handle, 
or manubrium mallei. Its sharp external margin is connected with the 
drum membrane by means of a thin interposed layer of cartilage. 

Ligaments of the Malleus. —The head of the malleus is attached to 
the under surface of the tegmen tympani by a thin suspensory ligament. 
From the anterior surface of the neck and from the long process (pro¬ 
cessus folianus) a short, thick, fibrous band, the anterior ligament, passes 
forward to the spina tympanica major and Glaserian fissure, to which 
it is attached. It surrounds the long process which is commonly ab¬ 
sorbed in later life. The posterior ligament seems really to be a posterior 
fasciculus of the lateral ligament. It extends backward from the pos¬ 
terior surface of the neck to be attached to the outer wall of the vault. 
These two ligaments,—the anterior and posterior,—though not quite in the 
same straight line, are sometimes spoken of as the rotary axis band of the 





22 


ANATOMY AND PHYSIOLOGY 


malleus. They prevent lateral displacement of the malleus, and account 
for the constancy of the short process as a landmark of the drum mem¬ 
brane: the short process may change its position— i.e., revolve as the 
malleus rotates about its axis band, but its location remains practically 
unchanged. The external ligament (ligamentum laterale) is attached to 
the outer surface of the neck above the short process, and spreads out, 
fan-shaped, to be attached to the outer bony wall of the vault. 

The Incus. —The body of the incus occupies the posterior half of 
the vault. Its posterior conical extremity, the short process, is lodged 
in a small depression, or facet (fossa incudis), in the posterior wall 
of the vault just below the aditus, or opening into the antrum. Both 
the fossa incudis and the articular surface of the short process are covered 
with thin layers of cartilage. The joint is held together by a strong cap¬ 
sular ligament and also by bands of fibrous tissue springing from the 
periosteum of the adjacent bone surfaces. Like the maileus, the incus is 
supplied with a suspensory ligament connecting its superior surface with 
the tympanic roof (Briihl) 1 . The anterior surface of the incus articulates 
with the head of the malleus. 

Articulation of the Malleus and Incus (Plate II, 25).—In describ¬ 
ing this joint it is necessary to allude once more to certain points in the 
anatomy of the bones. The posterior surface of the head of the malleus 
presents an irregularly oblong and spiral depression, or groove, extending 
from above downward and inward to the neck. The lower end of this 
groove is bounded externally by a projecting point of bone which exerts 
inward pressure upon a somewhat similar point of bone on the incus. 
This is called the cog, or tooth-process, of the malleus (Plate II, 22, C). 
On the anterior surface of the body of the incus is a spiral ridge which 
conforms to, and is received into, the spiral groove of the malleus. Internal 
to the lower end of the incudal ridge is a triangular projection of bone 
(23, D), which is spoken of as the cog, or tooth-process, of the incus. 
When the bones are in normal articulation, the tooth-process of the malleus 
is in contact with that of the incus (Plate II, 25). The result of this mech¬ 
anism is that when the malleus rotates inward,— i.e., when the hammer 
handle moves inward,—the incus is made to execute a similar inward 
rotation; when, however, the malleus is forcibly rotated outward,—as in 
sudden forcible condensation of the air in the tympanum, sneezing, Val¬ 
salva inflation etc.,—the cog, or tooth-process, of the malleus separates 
from that of the incus and the joint opens, so that excessive outward ex¬ 
cursions of the hammer handle are not necessarily accompanied by corre¬ 
sponding excursions of the long arm of the incus. By this provision, the 
stapes is guarded against the influence of extensive outward movements 
of the drum membrane which might otherwise result in dislocation of the 

1 Briihl states that there are distinct suspensory ligaments connecting both the malleus 
and incus with the tympanic roof. As there is a difference of opinion, however, as to 
the usual presence of a suspensory ligament of the incus, such a ligament is not included 
in Fig. 27, the author himself never having seen it. 




THE OSSICULAR CHAIN 


23 


stapes from the oval window. The opposed articular surfaces of the mal¬ 
leus and incus are lined with cartilage. The joint is provided with a strong 
capsular ligament and is further strengthened by strong fibrous bands. 

The long arm of the incus passes downward and backward into the 
cavity of the atrium. It is behind and more or less parallel with the ham¬ 
mer handle, but is not in contact with the drum membrane. It is shorter 
than the hammer handle, usually terminating about the mid-point of the 
latter, or even at a higher level. 

The Incudo-stapedial Joint is in the upper and posterior part of 
the atrium (see Fig. 27, and Plate II, 25). The rounded lenticular 
process of the incus and also the depression on the head of the stapes are 
covered with hyaline cartilage, and are held together by a capsular 
ligament. 

Articulation of the Stapes with the Fenestra Ovalis. —The 
margins of the oval window and the edges of the foot-plate of the stapes 
are covered with a thin layer of cartilage, which is said also to line the 
vestibular surface of the latter. These surfaces are held together by an 
annular ligament consisting of elastic and connective fibres derived from 
the periosteum of the inner margins of the fenestra and passing to the foot¬ 
plate of the stapes. The annular ligament is much wider in front than 
behind. 

So far as the writer knows, the ossicular chain is the only system of 
movable joints in the body the movements of which are not under the 
control of voluntary muscles. Aside from their minute size, the articular 
structures of these joints are the same in kind as are found in connection 
with the larger bones elsewhere. The movements of the ossicles, however, 
are initiated and maintained altogether by forces originating outside the 
body,— i.e., aerial vibrations set in motion by some vibrating body. The 
ossicular ligaments seem, therefore, to play a particularly important role, 
for they not only hold the joint surfaces in proper apposition, but serve 
to limit the activity of each ossicle to that particular form of motion to 
execute which is apparently its sole function. 

The Intra=tympanic Muscles. —The stapedius (Fig. 28) is a small 
muscle, about 5 or 6 millimetres long, the belly of which is enclosed 
in the bony canal of the eminentia pyramidalis. This canal is buried in 
the premastoid plate, lying in front of and parallel with the descending 
portion of the facial canal. Its upper extremity curves forward and 
appears upon the posterior wall of the tympanum as a very small bony 
prominence known as the eminentia pyramidalis (Fig. 28), the apex 
of which is just behind the oval window. The muscle arises from the 
walls of this canal, its fibres converging above into a tendon which emerges 
through a small orifice in its apex. From this point it passes forward to 
be attached to the head of the stapes and lenticular process of the incus. 
The canal of the pyramidal eminence communicates by a small orifice with 
the facial canal behind it, and through this a small branch of the facial 
nerve passes to supply the stapedius muscle. 


24 


ANATOMY AND PHYSIOLOGY 


The Tensor Tympani Muscle (Fig. 29)—This muscle is from 18 
to 20 millimetres long. It arises chiefly from the walls of an incomplete 
bony canal lying just above the osseous portion of the Eustachian tube, 
from the superior wall of the cartilaginous part of the Eustachian canal, 
and also by a few fibres from the inferior surface of the petrous bone. Its 


Stapedius muscle 



Hammer 

handle 


Eminentia 

pyramidalis 


Round window 



Oval window 


Pyramidal emi¬ 
nence and sta¬ 
pedius muscle 


Round 


Fig. 28.—Tympanum of infant six months old. (Left.) 


Fig. 29. —Tympanum of infant six months old. (I 


tendon passes backward and upward across the inner wall of the tympanum, 
and emerges from its bony canal in front of the anterior end of the oval 
window. Here it curves around the processus cochleariformis and passes 
outward to be attached to the upper part of the handle of the malleus 
(Fig. 29). It is supplied by the fifth nerve. 

The Lining Membrane of the Tympanum. — The mucous mem¬ 
brane lining the tympanic cavity is directly continuous through the Eu¬ 
stachian tube with that of the nasopharynx. Histologically it varies in 
character in different parts of the tympanum. Over the promontory it is 
of the cuboidal variety, while on the anterior half of the floor, and in the 
vicinity of the tympanic orifice of the Eustachian tube, it consists of cili¬ 
ated cylindrical cells (Politzer, Gruber). In the vault the cells are of the 
squamous variety, this type being continued into the aditus and antrum 
and persisting throughout the lining membrane of the mastoid cells. 
Beneath the epithelial, or mucous, layer are two layers of closely related 
connective-tissue fibres, the deeper of which is in contact with the osseous 
walls of the tympanum and constitutes their periosteal lining. The peri¬ 
osteal layer is very richly supplied with blood-vessels. 

Within the atrium the mucoperiosteal lining is for the most part 
smooth and very closely applied to the tympanic walls. In the vault, on 
the other hand, the mucosa is thrown into folds and reduplications, some 
of which hang down from the tegmen tympani and cover the bodies of the 
malleus and incus. 

The Pouches, or Pockets, of the Membrana Tympani. —There are 
three fairly constant and partially closed spaces (pockets, pouches) in 
relation to the drum membrane, which now must be described. The 




















THE POCKETS OF THE DRUM MEMBRANE 


25 


first is a small space lying between the neck of the malleus internally and 
Shrapnell’s membrane externally. It is bounded above by the external 
ligament of the malleus, internally by the neck of the malleus, below by 
the superior surface of the short process, and externally by the membrana 
flaccida. It is called Prussak’s space, its location being indicated upon 
the outer surface of the drum membrane by the boundary lines of the 
Rivinian notch (Fig. 26, B). Prussak’s space is said to communicate, by 
a small aperture in the external ligament of the malleus (its roof), with 
the attic, or vault. 

Stretching from before backward across the upper part of the cavity 
of the atrium, and passing between the handle of the malleus and the long 
arm of the incus, is a reduplication of mucous membrane which, by its 
attachment to the posterior surface of the neck and upper half of the 
hammer handle, is divided into two parts,—the anterior and posterior 
folds. The posterior fold is attached anteriorly to the neck and upper 
half of the handle of the malleus, and above and behind to the postero- 
superior margin of the drum membrane. Its dependent, free margin 
covers the chorda tympani nerve as it passes upward and forward toward 
the Glaserian fissure. Between this fold and the inner surface of the drum 
membrane is a pocket, or space, opening downward, which is known as 
the posterior pouch of the membrana tympani. The anterior fold 
is smaller, and extends from the neck and handle of the malleus to the 
antero-superior margin of the drum membrane. Between it and the 
inner surface of the drum-head is another, smaller space,—also opening 
downward,—the anterior pouch of the drum membrane. Prussak’s 
space is said to communicate with the posterior pouch behind, but has 
no communication with the anterior pouch. Both pockets of the drum 
membrane— i.e., the anterior and posterior—open below into the cavity 
of the atrium. 

With regard to the exact histological relations of the membranes enter¬ 
ing into the formation of these pouches, somewhat different views have been 
held. Von Troltsch, who first described the anterior and posterior pockets, 
regarded the membrane as a true reduplication of the membrana tympani, 
—this view being based upon his observation of certain fibres which he 
believed to be identical in structure with those of the fibrous lamina of the 
drum membrane. Politzer appears to regard them as reduplications of 
the inner, or mucous, layer of the drum membrane. Gruber in his investi¬ 
gations failed to find any fibres characteristic of the membrana propria, 
and regards the reduplications in question simply as folds of mucous 
membrane depending from the tympanic roof. 

The three spaces above described are all situated below the level of 
the external ligament of the malleus which forms the roof of Prussak’s 
space. Above this level the attic is itself divided into compartments 
more or less completely separated from each other by folds of mucous 
membrane. These spaces, while less constant in their arrangement than 
the pockets of the membrana tympani, must nevertheless be held in mind 


26 


ANATOMY AND PHYSIOLOGY 


on account of their possible influence upon the course of a suppurative 
process within the vault. 

The Attic Spaces. —The head of the malleus and body of the incus 
divide the attic into two chambers, an inner and an outer chamber. This 
partition is often completed by a fold of mucous membrane (the malleo- 
incudal fold) passing from the tympanic roof to the upper surfaces of the 
malleus and incus. This vertical fold incloses between its layers the sus¬ 
pensory ligaments of the malleus and incus, and extends from the anterior 
ligament of the malleus in front to the aditus ad antrum behind. The 
outer chamber of the attic is bounded internally by the bodies of the 
ossicles and the malleo-incudal fold, and externally by the outer bony wall 
of the vault. The outer chamber is subdivided by a horizontal fold of 
mucous membrane into an upper and a lower attic space. This horizontal 
fold is attached to the head of the malleus and body of the incus internally 
and to the osseous outer wall of the attic externally, and extends from the 
anterior ligament of the malleus in front to the short process of the incus 
and cella incudis behind. The lower attic space is bounded below by the 
ligamentum laterale mallei, which separates it from Prussak’s space. The 
upper attic space opens behind into the aditus ad antrum (Briihl). The 
membranous partitions between these spaces, while usually present, 
probably present many variations from those above described. They 
are said to contain many small apertures through which fluid may 
pass from one enclosure to another. This subdivision of the attic 
into compartments adds very materially to the gravity of a sup¬ 
purative process within the vault. It explains the surgical inadequacy 
of merely puncturing the drum membrane (paracentesis), and the 
importance of making a free incision through Shrapnell’s membrane 
and the soft tissues immediately behind it in all cases of acute purulent 
inflammation involving the vault. 

Vascular and Nervous Supply of the Tympanum.— Arteries. —The 
arterial supply of the middle ear is derived from the external and internal 
carotid arteries. 

From the external carotid are derived: (1) the tympanic branches of the 
ascending pharyngeal artery. This vessel gives off several small branches 
which enter the Eustachian tube, supplying the tubal muscles and mucous 
membrane. One or more of these enter the tympanum, pass upward over 
the promontory, and anastomose with the tympanic branches of the middle 
meningeal artery. (2) The tympanic braiiches of the middle meningeal artery. 
After entering the skull the middle meningeal gives off a branch (the 
petrosal) which enters the hiatus canalis Fallopii, anastomosing with 
the stylomastoid, and also several small branches which enter the tym¬ 
panum through the petrosquamosal suture. These latter supply the roof 
and part of the inner wall of the tympanum. (3) The tympanic branch of 
the internal maxillary enters the tympanum through the Glaserian fissure, 
supplying the mucous membrane of the anterior wall and drum membrane 
and anastomosing with the tympanic branches of the internal carotid 


TYMPANIC BLOOD-VESSELS 


27 


artery. (4) The stylomastoid artery (branch of the posterior auricular) 
anastomoses within the facial canal with the petrosal branch of the middle 
meningeal artery. It gives off several tympanic branches which enter 
the tympanum through small orifices in its posterior wall. It also sends a 
branch to the canal which terminates in the eminentia pyramidalis, sup¬ 
plying the stapedius muscle (Zuckerkandl). 

From the Internal Carotid Artery. —The tympanic branch of the internal 
carotid enters the tympanum through an aperture in the carotid canal 
and anastomoses with the tympanic branches of the internal maxillary 
and stylomastoid arteries. 

Veins. —The veins which remove the blood from the tympanic cavity 
correspond somewhat to the tympanic arteries. They leave £he tympanum 
by various routes,— i.e., (a) through the petrosquamosal suture, or minute 
foramina remaining after its obliteration, emptying into the veins of the 
dura mater; (b) through small foramina in the carotid canal, empty¬ 
ing into the carotid plexus; (c) by way of the Glaserian fissure, join¬ 
ing the veins about the temporomaxillary joint. There are also a large 
number of small veins which perforate the drum membrane at its 
periphery to join those of the external auditory meatus. Engorgement 
of these latter is the cause of the characteristic peripheral redness of 
the drum membrane, so often seen in tubotympanic congestion, or when 
the venous return flow has been impeded by continuous pressure upon 
the walls of the meatus, as by a speculum too large or retained in posi¬ 
tion too long. 

Nerves. —The nervous supply of the middle ear is derived chiefly from 
the glossopharyngeal , the sympathetic, and the trifacial. The tympanic 
branch of the glossopharyngeal (Jacobson’s nerve) is derived from its 
petrous ganglion, which is situated on the inferior part of the petrous 
portion of the temporal bone. It enters the tympanum through a small 
foramen in the tympanic floor, and, passing upward upon the promontory, 
divides into branches which are distributed to the round and oval windows 
and to the mucous membrane of the middle ear and the Eustachian tube. 
It also gives off branches of communication which lie in grooves upon the 
promontory and pass in different directions to their anastomotic connec¬ 
tions. This division of the tympanic (Jacobson’s) nerve into branches of 
distribution, together with its association with other nerves, constitutes 
the tympanic plexus. Its branches of communication are three in number. 
One of these passes downward and forward to unite with the tympanic 
branches of the sympathetic. A second communicating branch passes 
upward and forward to join the large superficial petrosal nerve. A third, 
receiving a small branch from the otic ganglion, passes upward in the 
substance of the petrous bone as the small superficial petrosal nerve. It 
receives in passing a filament from the ganglionic enlargement of the facial 
nerve. 

The Sympathetic. —The tympanic branches of the sympathetic (nervi 
carotici-tympanici) are derived from the carotid plexus. They enter the 


28 


ANATOMY AND PHYSIOLOGY 


tympanum through small openings in the carotid canal, and there unite 
with filaments of the communicating branches of Jacobson’s nerve, aiding 
in the formation of the tympanic plexus. 

The Trifacial .—This nerve contributes to the nerve supply of the 
middle ear chiefly through the otic ganglion, which supplies two small 
branches, one to the membrano-cartilaginous Eustachian tube and the 
other to the tensor tympani muscle. 

The stapedius muscle is supplied by a branch of the facial, the tensor 
tympani by a small branch from the otic ganglion. 

The chorda tympani nerve traverses the tympanum without supplying 
it. It leaves the facial canal a little above the stylomastoid foramen, and 
passes obliquely upward and forward through a canal in the premastoid 
plate to enter the tympanum. It passes forward through the upper part 
of the atrium,—between the hammer handle and the long arm of the 
incus,—and leaves the tympanum at the Glaserian fissure through a 
canal known as the iter chordae anterius. In its passage across the tym¬ 
panum it is covered by the fold of mucous membrane which enters into 
the formation of the posterior pocket of the drum membrane. 

The Eustachian Canal. —The Eustachian tube connects the cavity 
of the tympanum with that of the nasopharynx, and forms a very impor¬ 
tant part of the sound-conducting apparatus. Structurally it is some¬ 
what analogous to the external auditory meatus in that it consists of two 
parts,—(1) an osseous and (2) a membrane-cartilaginous portion. Its 
length in the adult varies from 31 to 38 mm. (about lfi to \y 2 inches), 
of which about one-third is bony and two-thirds fibrocartilaginous. The 
two portions of the tube are not quite in the same straight line, their point 
of junction forming an obtuse angle, opening downward. The general 
direction of the canal from the tympanum to the nasopharynx is forward, 
inward, and downward,—so that its pharyngeal orifice is anterior to, and 
on a lower level than, the tympanic orifice. The tube is somewhat ex¬ 
panded at either end, the vertical diameter of the tympanic orifice being 
from 3 to 4 mm., while that of the pharyngeal orifice is 5 to 8 mm. The 
narrowest part of the tube is where the bony and cartilaginous portions 
join (the isthmus), at which point the calibre of the bony tube is not more 
than \y 2 to 2 mm. There are, however, parts of the. membrano-cartilagi¬ 
nous tube in which the calibre is made even less than this by approxima¬ 
tion of the anterior and posterior walls. 

The osseous portion of the Eustachian tube extends from the 
anterior wall of the tympanum forward, inward, and downward through 
the upper and outer portion of the os petrosum. It is in immediate rela¬ 
tion above with the canal for the tensor tympani muscle, this being roofed 
over by a continuation of the tegmen tympani. Internally it is separated 
by a thin plate of bone from the canal for the internal carotid artery. 
From its tympanic orifice the calibre of the tube becomes gradually smaller 
reaching its minimum diameter at its anterior, or inner, extremity, which 



EUSTACHIAN TUBE 


29 


presents somewhat roughened edges for the attachment of the cartilagi¬ 
nous portion of the canal. 

The membrano-cartilaginous portion of the Eustachian tube 
is attached to the base of the skull, and at the isthmus rests in the groove 
between the inferior border of the greater wing of the sphenoid and the 
petrous portion of the temporal bone. It commences at the anterior 
inner end of the bony canal, and from this point extends forward, inward, 
and downward to its orifice in the lateral wall of the nasopharynx. Its 
cartilaginous frame is not complete,—only its posterior wall, roof, and 
upper part of the anterior wall being cartilaginous, the remainder being 
completed by fibrous tissue (Fig. 30). Its posterior (median) wall is 
formed by a plate of fibrocartilage which becomes wider as it extends for¬ 
ward and inward, its pharyngeal margin causing a somewhat vertical 
projection upon the lateral wall of the nasopharynx. This projection, or 


Cartilage of roof 


Posterior, or median, 
cartilaginous plate 


Floor of membranous canal 


Fig. 30.—Transverse section of Eustachian tube (after Schwalbe, reduced). 


Cartilaginous plate of 
anterior, or lateral, wall 

Tensor palati muscle 

Anterior, membranous wall 



ridge, forms the posterior wall of the pharyngeal mouth of the tube, and 
the anterior wall of the fossa of Rosenmuller. The upper margin of the 
cartilage of the posterior wall curls forward and then downward, being 
thus continuous with the roof and cartilaginous plate of the anterior wall. 
The narrow groove between the anterior and posterior plates forms the 
roof of the canal. The anterior (external) cartilaginous plate is narrow 
and forms only one-fifth of the anterior wall of the tube. Below this the 
anterior wall and floor are formed by a dense fibrous membrane (tunica 
propria) which is richly supplied with blood-vessels. The fibrous layer is 
continuous with the perichondrial lining of the cartilaginous portion of the 
tube (Rudinger). 

The mucous membrane lining the Eustachian tube is of the ciliated 
cylindrical variety. In the pharyngeal end of the canal it is thicker and 
more loosely applied, and upon the anterior (membranous) wall it forms 
several longitudinal folds which admit of a certain degree of expansion of 
the tube without stretching the mucosa. 

Much has been written, and many varying views advanced, as to the 










30 


ANATOMY AND PHYSIOLOGY 


patency of the Eustachian tube when the palatal muscles are at rest. 
Since post-mortem conditions, as shown by cross-sections of the tube, 
can not be relied upon as determining the condition of the parts in the 
living subject, it seems safest to confine one’s statements to demonstrable 
facts. In all parts of the membrano-cartilaginous tube its vertical diam¬ 
eter far exceeds the lateral, which in most situations is obliterated by the 
contact of opposing surfaces. Owing to the absence of a complete car¬ 
tilaginous frame, the anterior (membranous) wall is in contact with the 
posterior wall. In the upper part of the tube, however, the narrow car¬ 
tilaginous plate which forms part of the anterior wall should tend to pre¬ 
serve the patency of this part of its lumen. It is this upper portion of the 
' lumen of the membrano-cartilaginous tube which represents the direct 
continuation of the bony canal. It is probable that in health the lumen of 
the osseous canal is always patent; and that its anterior extremity, acting 
as a support, aids in maintaining the patency of the contiguous portion of 
the membrano-cartilaginous tube. The patency of the pharyngeal end of 
the tube is also, in all probability, maintained by its better cartilaginous 
support in this situation. Between these two terminal portions of the 
fibrocartilaginous tube, it seems probable that its anterior and posterior 
walls are for the most part in contact except when acted upon by the 
palatal muscles. 

Anatomical Differences Between the Eustachian Tubes of 
the Adult and the Infant at Term. —In the new-born infant the Eusta¬ 
chian canal presents the following marked variations from the adult type: 
(1) It is very much shorter, measuring not more than 14 or 15 mm. 2 (33 
to 38 mm. in the adult). (2) The tympanic orifice and the calibre of the 
bony tube are quite as large as in the adult. The whole canal is, therefore, 
in proportion to its length much wider. (3) The two portions of the tube 
(i.e., the membranous and the bony) are more nearly in the same straight 
line, so that there is no demonstrable angle at their point of junction. (4) 
The whole tube is nearly horizontal in direction, so that, while the pharyn¬ 
geal orifice in the adult is on a lower level by 12 to 14 mm. than the tym¬ 
panic orifice, 3 it is on the same plane as the latter in the infant at term. 
(5) The pharyngeal mouth of the tube in the infant at term is on the same 
level as the hard palate,— i.e., just behind the choanse,—whereas in the 
adult it is not less than 10 mm. above the hard palate. 


2 The statement found in many text-books, that the Eustachian canal of the infant 
at birth is 18 to 20 mm. long, is not correct. Remembering that the infant tube is 
nearly or quite horizontal in direction, examination of the base of the skull of an infant 
at term seems to demonstrate clearly that the length of the entire tube can not at this 
period exceed 14 or at most 15 mm. 

3 The statement of Politzer (Diseases of the Ear, p. 38), repeated by Bruhl (Atlas 
of Otology, p. 37), that the tympanic orifice is in the adult on a level about 2.5 cm. 
higher than the pharyngeal orifice, is obviously incorrect, since, with Politzer’s esti¬ 
mated length of 34 to 36 mm., this difference in the level of its two extremities would 
bring the direction of the canal into a plane much nearer the vertical than it is known 
to occupy. 






MUSCLES OF THE EUSTACHIAN TUBE 


31 


The above anatomical differences, while undergoing fairly rapid modi¬ 
fication with the growth of the child, may be accepted as characteristic 
of the tubal type in infancy as compared with the adult type. 

Muscles of the Eustachian Tube. —When at rest, the Eustachian 
canal is supposed to be practically a closed tube. At frequent intervals, 
however, it is made to dilate in response to the action of two muscles, 
which must, therefore, be briefly described. 

The levator palati arises from the anterior part of the under surface 
of the petrous bone, and passes obliquely downward and inward along 
the outer wall of the nasopharynx to be attached to the posterior sur¬ 
face of the soft palate. In its course toward its palatal attachment, 
some of its fibres are attached to the floor of the membranous canal. 
Its contraction serves to elevate the soft palate and to dilate the Eusta¬ 
chian tube by elevating its floor. The levator palati is supplied by the 
great superficial petrosal nerve (from the superior maxillary branch of 
the 5th). 

The tensor palati muscle consists of two portions, which are some¬ 
times spoken of as the vertical and horizontal portions respectively. The 
vertical portion arises from the scaphoid fossa at the base of the pterygoid 
plate, from the spine of the sphenoid, and from the anterior membranous 
wall of the Eustachian canal. These fibres unite to form a broad, thin 
muscle, which passes downward and slightly forward to the hamular 
process of the internal pterygoid plate. The muscle then winds around the 
hamular process and passes inward (horizontal portion), to be attached 
to the anterior surface of the soft palate. Its contraction elevates the soft 
palate and dilates the Eustachian tube by drawing its anterior wall down¬ 
ward and forward and thus away from the posterior wall. This muscle is 
supplied by the otic ganglion. 

There is still another small muscle, the salpingo-pharyngeus, the con¬ 
traction of which influences the calibre of the tube. It arises from the 
tubal prominence, or pharyngeal end of the posterior cartilaginous plate 
of the tube, and passes backward to be inserted into the posterior pharyn¬ 
geal wall. 

The Mastoid Process (Plate III).—The mastoid process is the large 
conical protuberance of bone which projects downward behind and below 
the bony meatus. It is bounded above by the tegmen antri, which sep¬ 
arates it from the middle cerebral fossa. The interior of the upper part of 
the mastoid process communicates with the tympanic vault, which lies 
immediately in front. Below this it is separated by the dense bony plate 
of the posterior canal wall from the osseous meatus. Interiorly it projects 
downward below the level of the floor of the meatus, terminating in the 
conical process known as the tip (Fig. 31, 6). The outer surface is convex 
(31, a) and more or less roughened for the attachment of muscles. The 
inner surface of that portion of the mastoid lying above the floor of the 
meatus forms part of the posterior cerebral fossa. It presents the deep 
groove (32, a) which lodges the descending portion of the lateral sinus. 


32 


ANATOMY AND PHYSIOLOGY 

J 

The position of this groove in its relation to the tympanum varies greatly 
in different skulls. It is one of the most important surgical relations of 
the tympanum, and will be considered more fully in a later chapter deal¬ 
ing with the surgical anatomy of the temporal bone. The inner surface 
of the tip—that portion of the mastoid which projects downward below 
the base of the skull—forms the outer boundary of a groove, running 
from before backward, for the attachment of the posterior belly of the 
digastric muscle (31, c). 

The mastoid process consists of an outer shell, or cortex, of dense 
compact bone, inclosing a central chamber, which may be subdivided into 
pneumatic spaces or filled with diploic tissue. Accordingly two types 
are recognized, viz. : 

(1) The pneumatic (Fig. 34), in which the interior is subdivided into 
distinct spaces, which are lined with mucous membrane, and may be of 
very considerable size. In this variety there is invariably a large cell at 
the tip, in which pus is apt to collect during the course of a suppurative 
mastoiditis. 

(2) The diploic mastoid (Fig. 35).—In this variety, instead of dis¬ 
tinct, pneumatic spaces, we find the interior of the mastoid filled with 
cancellous tissue, somewhat resembling that w r hich occupies the space 
between the inner and outer plates of the cranial bones. In the dried 
bone this tissue appears as if composed of very small, thin-walled osseous 
cells. In the living subject, as seen during an operation upon the mastoid, 
it consists of a vascular, spongy tissue offering only moderate resistance to 
the rongeur or curette. Even in bones of this type there is usually present 
a single large cell at the tip. Between the two varieties above described, 
there are many bones which present the characteristics of each,— i.e., 
pneumatic spaces and diploic tissue occupying different parts of the same 
bone. 

Still another type of bone has been described as the sclerotic mastoid. 
In this variety there may be throughout the greater part of the mastoid 
process complete absence both of pneumatic spaces and of diploic tissue, 
their place being occupied by fairly compact bone. This solidification 
sometimes occurs as a pathological change resulting from chronic middle- 
ear suppuration of long standing. There are undoubtedly cases, however, 
in which the mastoid is practically filled with a solid mass, in spite of the 
fact that the tympanum may present no evidences of having been the seat 
of disease. The accompanying illustration (Fig. 36) was made from ia 
specimen prepared by the author. That there had been ho prolonged 
suppurative process within the tympanum was shown by the condition of 
the ossicles and drum membrane, which were intact and normal. 

The Antrum.— There is one space, usually of considerable size, which 
is always present, viz., the so-called mastoid antrum. This is the large 
space situated in the upper and anterior part of the mastoid process imme¬ 
diately behind the tympanic vault. There can be no doubt that this space 
forms part of the tympanic cavity. Its roof is directly continuous with 


THE MASTOID PROCESS 


33 


Plate III. 



Fig. 31. —Temporal bone, outer surface; a, mas¬ 
toid process; b, tip of mastoid; c, groove for posterior 
belly of digastric muscle. 



Fig. 33.—Vertical section of temporal 
bone passing through aditus ad antrum; 
a, aditus, leading forward into tympanic 
vault. 



Fig. 35. — Section through mastoid 
process of diploic type ; a, antrum. 

3 



Fig. 32, —Temporal bone, inner surface;’ a, 
groove for sigmoid sinus,— i.e., descending part 
of lateral; b, tip of mastoid; c, internal auditory- 
meatus. 



Fig. 34. —Section through mastoid proc¬ 
ess of pneumatic variety, showing typical 
pneumatic spaces or cells. 



Fig. 36. — Section through mastoid 
process of sclerotic variety. 









34 


ANATOMY AND PHYSIOLOGY 


that of the vault, from which it is differentiated only by the triangular 
constriction known as the aditus ad antrum (33, a). The antrum is fully 
developed in the new-born,— i.e., before even a rudimentary mastoid can 
be demonstrated. Later it is surrounded and appropriated by the devel¬ 
oping mastoid process. 

In this brief description of the mastoid process, the author has deemed 
it best to deal only with those general characteristics a knowledge of which 
is absolutely essential to the intelligent study and appreciation of the 
commoner acute middle-ear lesions. He has endeavored to emphasize 
the fact that the antrum is not to be considered separately as one of the 
mastoid cells, but rather as the posterior end of the tympanic vault. This 
method of describing it enables the student more easily to remember its 
exact position and its surgical significance. It has the further advantage 
of being, from the stand-point of its development, the only correct view; 
for even in fetal life— i.e., long before even a rudimentary mastoid is 
present—the antrum is an easily demonstrable cavity. 


Physiology of Sound-Conduction. 

It is impossible to consider the process of sound-conduction without 
having in mind both the physics of sound and the physics and physiology 
of the conducting mechanism. With special students of otology, more or 
less familiarity with the physics of sound may be assumed. For the busy 
medical practitioner, however, it may not be amiss to recall briefly certain 
elementary, though perhaps forgotten, facts upon which our knowledge 
of the physiology of sound-conduction is based. 

Sound is a form of motion produced by some vibrating body. A sound¬ 
wave is a series or chain of alternate condensations and rarefactions in the 
surrounding air, by which the vibratory movements of the sounding body 
are conveyed to the drum membrane. When these vibrations occur 
singly or follow each other irregularly, the resulting sound is discordant 
and is spoken of as a noise. When the vibrations recur rhythmically or at 
regular intervals, and with sufficient rapidity, a musical tone results. 

The pitch, or relative position of sound in the musical scale, depends 
upon the rapidity with which the vibrations follow one another, the pitch 
being raised as the number of vibrations per second is increased. The 
human ear normally appreciates musical tones between two extremes of 
vibration rapidity, the lower tone limit being eighteen vibrations per 
second, and the upper tone limit somewhere between 32,500 and 50,000 
vibrations per second. Vibrations recurring rhythmically at a rate of less 
than eighteen per second may be heard as separate impulses, but are not 
heard as a continuous musical tone. Taking any note in the musical 
scale, c.g., C- 2 , 32 double vibrations,—by doubling the number of vibra¬ 
tions we may produce a tone one octave higher. Thus 32, 64, 128, and 
256 double vibrations per second represent C tones one octave apart. 
Pitch, then, is determined solely by the number of vibrations per second 



PHYSICS OF SOUND 


35 


I I 
1 I 
' I 


I I 
I I 
I I 
1 I 


KJ 


1 1 
i i 
11 

:! 
i l 
i i 
i i 
i i 
i i 
i i 
i i 
i i 
, i 


Intensity.— The intensity with which a sound-wave impresses the per¬ 
ceptive mechanism depends upon its amplitude of vibration. Taking for 
example a tuning-fork such as is represented by Fig. 37. a double vibra¬ 
tion includes the passage of the prong from a to b , its 
recoil to c, and its return to a, its position of rest. The b a c 
line b-c represents what is called the amplitude of vibra¬ 
tion. Supposing this to represent its vibration when set 
in motion by a moderate tap, a more vigorous blow will 
result in more extensive movements, the amplitude of 
vibration being greater and the intensity of the sound 
being correspondingly increased. This is in accordance 
with the physical law which declares that the intensity 
of sound is 'proportional to the square of the amplitude. 

Timbre. —There is a third property of musical sound, 
that peculiar quality by which we are able to distinguish 
tones of the same pitch as produced by different musi¬ 
cal instruments; e.g., the C tone of the piano, of the 
violin, and of the human voice. For an explanation of 
this quality of sound, and of the harmonics or overtones 
to which it is due, the reader is referred to anv of the 
standard works on physics. 

Sound-Conduction. —The Auricle and External Audi¬ 
tory Meatus. —To most of the lower animals the auricle 
is undoubtedly of great value in aiding them to concen¬ 
trate their auditory effort at will upon some particular 
sound by turning the auricles in the direction from which 
it comes. In man, on the other hand, the auricle has 
lost much of its importance as a part of the conducting 
apparatus since the auricular muscles have lost the 
property of voluntary contraction,—in other words, since 
man has lost the power of moving the auricles at will. 

That he still retains an intuitive appreciation of their 
function is shown by the impulse which leads the hard- 
of-hearing instinctively to draw the ear forward toward 
the source of sound and to augment its concavity by 
that of the hollow of the hand. While it is now recog¬ 
nized that fairly good hearing is not inconsistent with 
complete loss of the external ear, it can not from this 
be assumed that the auricle is without influence upon 
the auditory function. Politzer has called attention to Fig. 37 .—Tuning-fork, 
the fact that b}^ filling the concha with wax, even 
though the orifice of the external auditory canal be left open, we reduce 
considerably the acuteness of audition; whereas obliteration of the other 
auricular depressions— e.g., the fossa of the helix, fossa of the antihelix, 
etc.—does not influence the hearing appreciably. The concha, therefore, 
must be regarded as in man the most important part of the auricle, its 













36 


ANATOMY AND PHYSIOLOGY 


function being to receive and carry forward the sound-waves to the inner 
surface of the tragus, by which they are deflected into the external auditor} 7 
meatus. The external auditory canal presents curves and variations in 
calibre in different parts, which undoubtedly have to do with the proper 
focusing of sound-waves upon the membrana tympani. These anatomical 
pecularities, however,—provided that its lumen is not completely occluded, 
—seem to be less essential to perfect hearing than almost any part of the 
conducting apparatus. Individuals with abnormally narrow auditory 
canals seem often to hear equally as well as others with canals of normal 
calibre. The author has seen several cases in which the bony meatus was 
very considerably narrowed in one or more of its diameters by exostoses 
from one or other of its walls, in which no appreciable impairment of 
hearing could be demonstrated. Another phenomenon with which every 
aurist is familiar is the excellent hearing power frequently exhibited by 
individuals whose auditory canals are apparently filled with cerumen, 
exfoliated epithelium, or other foreign substances. Whether in such cases 
the obstructing mass vibrates in unison with the sound-waves from without 
and thus transmits them to the column of air between it and the drum 
membrane, or the sound-waves are projected through some space between 
the foreign body and one of the canal walls, may be a debatable 
question. The latter hypothesis seems the more plausible. Sound¬ 
waves, then, are collected in the concha, whence they are deflected by 
the inner surface of the tragus into the external auditory canal, by 
which in turn they are conveyed to the outer surface of the membrana 
tympani. 

The Drum Membrane. — In the membrana tensa we have an ideal 
medium for the transmission of sound-waves to the ossicular chain. It is 
a tense, inelastic, fibrous membrane, drawn inward at the centre by its 
attachment to the lower half and extremity of the hammer handle, and 
presenting, therefore, a somew r hat funnel-shaped concavity toward the 
meatus. From the central depression at the umbo to its peripheral attach¬ 
ment, the membrane is slightly bowed or curved in the direction of the 
meatus. This outward curvature of the normal membrane is not without 
influence upon its value as part of the conduction mechanism, Helmholtz 
having established by experiments the greater resonance of curved mem¬ 
branes as compared with flat ones. 

If the drum membrane were highly elastic it would respond easily to 
sound-waves, but would hold these and other vibrations due to harmonics 
or overtones, after the original stimulus had spent itself; and these after¬ 
tones would interfere with the proper transmission of sound-waves immedi¬ 
ately following. But the membrana tensa is a comparatively unyielding 
and inelastic structure, responding readily to all forms of sonorous stimuli 
but returning rapidly to a condition of rest as soon as it ceases to be acted 
upon by sound-waves from without. As with all stretched membranes 
and sonorous bodies generally, the membrana tensa has a fundamental 


THE FUNCTION OF THE MEMBRANA TUMP AN I 


37 


note of its own. By this is meant that the drum membrane, if set in motion 
by a light tap, or any force momentarily bending it, must execute a series 
of to-and-fro movements, or vibrations, before it can return to a condition 
of rest; and that these movements will be rhythmic in character and will 
take the form of sonorous vibrations having a constant rate of rapidity 
per second; in other words, they would if sufficiently extensive and pro¬ 
longed produce a musical tone of constant pitch, its fundamental tone. 
One disadvantage of a loud fundamental note in the drum membrane 
would be the confusion which would inevitably result if it were acted 
upon by sound-waves having the same number of vibrations per second. 
It must be remembered that the drum membrane is capable not only 
of responding to all kinds of sonorous impressions, but of transmitting 
several sound-waves simultaneously. One can readily appreciate, there¬ 
fore, that a fundamental tone of any part of the conducting mechanism 
which would respond loudly even to overtones of the same pitch might 
cause great disturbance of function. Against this result, the handle of 
the malleus acts as a control mechanism, the effect of its attachment 
to the drum membrane being somewhat analogous to the pressure of 
a finger against the prong of a vibrating tuning-fork,— i.e., the vibra¬ 
tions due to the fundamental tone of the drum membrane are immedi¬ 
ately overcome by the inertia of the attached ossicular chain, leaving 
the membrana tensa free to receive and transmit new sound-waves from 
without. 

The Ossicular Chain .—According to the commonly accepted theory, 
sound-waves striking upon the membrana tympani are by it communi¬ 
cated to the ossicular chain, by which in turn they are transmitted through 
the foot-plate of the stapes to the labyrinthine fluids. Each excursion in 
either direction of the stapes is accompanied by a corresponding movement, 
or displacement, of the fluid in the vestibule, and in this way fluid waves 
are inaugurated which finally impress the terminal filaments of the audi¬ 
tory nerve. For the exercise of these passive movements, the drum mem¬ 
brane and ossicles constitute a perfectly adapted mechanism. The ossicles 
form a system of finely adjusted and sensitive levers which respond in¬ 
stantly to the slightest movements of the drum membrane. The handle 
of the malleus being the only part of the ossicular chain directly attached 
to the membrana tympani, it is through this process that the movements of 
the drum-head are transmitted to the .ossicles. The handle of the malleus 
is longer than the long arm of the incus; so that, according to the laws 
governing leverage, with each inward excursion of the hammer handle, the 
long arm of the incus moves inward, carrying with it the stapes through a 
shorter distance but with greater force. This provision has a particularly 
important bearing upon the transmission of the lower musical tones, which 
arc produced by vibrations of large amplitude but relatively little force. 
The funnel-shaped concavity of the drum membrane and its outward 
curve from centre to periphery have also an important bearing upon the 


38 


ANATOMY AND PHYSIOLOGY 


function of the conducting mechanism,—such a membrane, according to 
Helmholtz, transmitting low vibrations of smaller force than would a flat 
membrane. Apparently, therefore, the ossicular chain is most essential in 
transmitting the lower tones of the musical scale,—tones produced by 
vibrations of large amplitude but little force, which the ossicular levers 
convert into vibrations of smaller amplitude but of greater force. The 
higher tones, on the other hand, are produced by sonorous vibrations of 
smaller amplitude, but whose relatively greater force is capable of inaugu¬ 
rating a fluid wave within the labyrinth without augmentation of force 
through the leverage system of the ossicular chain. With this theorem 
in mind, we should be at no loss to explain the impairment of hearing for 
the lower tones of the musical scale which invariably attends any severe 
lesion of the conducting mechanism. 

The relative movements of the different ossicles have been investigated 
by Helmholtz, Politzer, and others. According to their experiments, the 
maximum excursion of the hammer handle (at umbo) which can be in¬ 
duced by condensation and rarefaction of the air in the external auditory 
canal is % mm., the maximum movement of the stapes being %4 to Ms mm. 
These measurements throw light on the influence of leverage on the ossicu¬ 
lar movements, and furnish additional proof that the ossicles move sepa¬ 
rately and individually as parts of a movable chain, and never in unison 
as parts of a rigidly bound whole. It must be understood, however, that 
the measurements given represent only the excursions which may be 
experimentally induced, Riemann having proved by mathematical calcu¬ 
lations that the largest excursion of the stapes possible in response to sound¬ 
waves would be smaller than the eye could appreciate. 

Another view, which has been entertained, as to a possible pathway 
for sound-waves is that they may reach the labyrinth by way of the round 
window. Thus, Politzer 4 states that “the vibrations of the drum membrane 
are transmitted to the labyrinth partly through the ossicles by means of 
the foot-plate of the stapes, and partly through the air in the tympanic 
cavity to the membrane of the fenestra rotunda.” The writer can not 
conceive how in a healthy ear it is possible for the membrane of the round 
window to take so direct a part in the transmission of sound-waves. To 
accept such a view, it would be necessary to assume that, with each in¬ 
ward movement of the membrana tympani, the membrane of the round 
window is also forced inward by condensation or displacement of the air 
in the tympanic cavity, an untenable hypothesis. The membrane of the 
round window moves inward toward the lumen of the scala tympani only 
during the period of rarefaction of sound-waves,— i.e., during the period 
in which the stapes moves outward. In other words, its function seems 
purely one of compensation for the movements of the stapes, thus preserv¬ 
ing the stability of intralabyrinthine pressure. 


4 Diseases of the Ear, last English edition, p. 57. 




ROLE OF THE TYMPANIC MUSCLES 


39 


The Tympanic Muscles .—The function of the tensor tympani and 
stapedius muscles has been the subject of a great deal of controversy. 
Contraction of the tensor tympani, drawing the hammer handle and drum 
membrane inward, renders the latter more tense. Contraction of the 
stapedius draws the head of the stapes backward and the anterior end 
of the foot-plate of the stapes somewhat outward into the niche of the 
oval window. Acting together, the two muscles oppose each other, one 
drawing the ossicles inward, the other tending to draw the stapes out¬ 
ward. In this way it is believed that they may constitute a sort of con¬ 
trol mechanism, guarding the labyrinth, on the one hand, from the effect 
of loud or explosive noises which might drive the stapes violently in¬ 
ward, and, on the other, neutralizing the effect of sudden and forcible 
condensation of the air within the tympanum which might cause ex¬ 
cessive excursions of the hammer handle and drum membrane in the 
other direction. 

Another theory is that which was proposed by Mach as long ago as 
1863. According to this view, the muscles act as an accommodation appa¬ 
ratus, varying and regulating the tension of the conducting mechanism 
according to the requirements of different sound-waves, and also enabling 
the individual by an effort of will to select and follow certain sounds. 
This view, with some modifications, has received the support of most 
later observers. Henson, in 1876, showed by experiments upon living ani¬ 
mals that the tensor tympani muscle not only contracts in response to 
sound-waves, but executes a distinct contraction for each particular 
sound; and further that its contractions were stronger for high tones 
than for the lower tones of the musical scale. Giving these facts greater 
significance were the later experiments of Poliak, which proved that 
after removal or destruction of the cochlea in living animals the tensor 
tympani no longer contracts except in response to electrical stimulation. 
While absolute proof as to their function is beyond our reach, this 
view—viz., that different sound-waves require variations in the tension 
of the sound-conducting mechanism for their perfect transmission, and 
that such variations are controlled and regulated by the tympanic 
muscles—is in harmony with laboratory investigations, and furnishes 
the only hypothesis which seems adequately to explain these perfect 
little muscles. 

A question which is still the subject of occasional discussion, and 
apparently with little prospect of definite solution, is whether sound-waves 
are in any degree conducted through the ossicles and labyrinthine fluids 
by molecular motion, or altogether through vibration of these structures 
en masse. The fact that the higher musical tones are in many cases veil 
perceived in spite of advanced obstructive lesions in the conductive mech¬ 
anism, is by some regarded as pointing to a possible transmission of these 
sounds by molecular processes, rather than by mass movements of the 
ossicular chain. In this regard the following expression of belief by the 


40 


ANATOMY AND PHYSIOLOGY 


late Professor Bezold 5 of Munich is of interest: “I share the conviction 
. . . that not molecular movements, but mass movements of the con¬ 
ducting chain, together with the labyrinthine water column, transmit 
the sound-waves from the air; ... I am, moreover, on the side of 
those physiologists who regard bone conduction as osteotympanic. In 
other words, in conduction through bone, the excitation of the auditory 
nerve takes place exclusively with the aid of the sound-conducting appa¬ 
ratus, vibrating with the bone.” This view, while not final, probably 
expresses the belief of a majority of otologists and physiologists to-day. 


5 Archives of Otology, vol. xxxv, No. 3, p. 217. 






CHAPTER II. 

PHYSICAL EXAMINATION OF THE PATIENT. 

Under this heading should be included a short but comprehensive 
history of the case; and this should include not only all essential data as 
to the present attack, but also an account of any previous conditions or 
disorders which may throw light on the aural disease. 

Age, Occupation, Habit, Heredity. —Age has a particularly impor¬ 
tant bearing upon aural disease and should always be taken into account. 
The patient’s occupation and habit or mode of life— e.g., environment, 
excessive addiction to alcohol or tobacco, habitual overwork, dissipation, 
etc.—should be kept in mind as having a possible bearing upon the aural 
affection. The question of heredity is apt to be considered chiefly in 
connection with adult patients suffering from impaired hearing. It might 
be taken into far more useful account in our dealing with the children of 
the deaf or hard-of-hearing, with whom especial effort should be made to 
correct any conditions predisposing to aural disease. 

Previous Historv.—This should include a record of (A) any consti- 
tutional disease, inherited or acquired,— e.g., syphilis or tuberculosis. 
(B) Diatheses, of which gout and rheumatism are the most impor¬ 
tant. That rheumatism is the indirect cause of many cases of ecolog¬ 
ically obscure aural disease there can be no doubt; and there are some 
observers (Buck, 0. Wolf, Von Urcherman) who believe that acute rheu¬ 
matism is not infrequently manifested as a primary lesion within the 
tympanum.- (C) The acute infectious diseases, either in childhood or 
in later life. At least 8 per cent, of all cases of scarlet fever, diphtheria, 
and measles develop some form of middle-ear inflammation. Particularly 
are many cases of chronic suppurative otitis media traceable to such lesions 
early in life. (D) Previous attacks of acute otitis media. There, are 
many children whose histories are completely negative as to infectious 
diseases who have, however, experienced two or more attacks of acute 
tympanic inflammation. Recurring attacks of aural pain and discharge, 
for which no exciting cause can be assigned, should always suggest tne 
possibility of some abnormal condition within the nasopharynx. Certainly 
such a history should make one more guarded in one s prognosis until the 
nasopharyngeal lesion, whatever it may be, has been corrected. 

History of the Present Attack. —This should begin with a statement 
of the disease to which the aural disorder was secondary, or with the 
exciting cause. In order to fix as nearly as possible the date of the onset, 
we should begin with the initial symptom—pain, deafness, tinnitus—and 
the date on which it was first experienced by the patient. In acute cases, 
next to the initial symptom, it is important to learn if possible the time 
which has elapsed between the onset of the attack and the appearance o 


42 


EXAMINATION OF THE PATIENT 


the aural discharge, provided this be present. The importance of this lies 
in the fact that in acute tympanic disease the prognosis is, as a rule, more 
favorable in those cases in which spontaneous rupture of the drum mem¬ 
brane follows quickly upon the initial symptom than in cases in which it is 
delayed several days or a week. Further than this but little can usually be 
learned beyond what the physician's examination will bring to light,— 
unless, of course, the patient has been under the care of a trained observer. 
It is, of course, well in the case of a seriously ill patient to inquire as to 
whether rigors, profuse sweating, or sudden and pronounced alterations of 
temperature have been noticed ; but the statements of the family or attend¬ 
ants in regard to such symptoms are rarely to be relied upon. In other 
words, the physician is usually obliged to await the results of his own 
observation on these points. 

In cases of chronic aural disease the history may extend over a period 
of months or as many as ten or twenty years. Obviously such cases require 
a more thorough weighing of individual symptoms, their sequence, and 
relative severity or prominence in different stages of the disease. 

To epitomize: The main points of interest in the history of a patient 
suffering from tympanic disease group themselves about the following 
facts: 

(1) The primary disease to which the otitis was secondary, or the 
exciting cause. 

(2) The date and character of the onset. 

(3) In acute cases, the date and character of the discharge. 

(4) The presence or absence of symptoms of constitutional disturb¬ 
ance,—nausea, vomiting, rigors, septic temperature, etc. 

(5) In chronic cases, the sequence of the various symptoms, and their 
relative severity in different stages of the disease. 

(6) The course of the disease as shown by subsidence or persistence, 
increase or diminution of symptoms. 

From what has been written, it may seem that the writer has proposed 
a somewhat voluminous history. This, however, is not necessary, it 
being quite possible to include all that is of practical importance within 
a comparatively small space. To facilitate this, some form of printed his¬ 
tory blank is almost essential. The writer has found two forms of history 
cards useful,— i.e., one for office histories, used mostly in cases of chronic 
aural disease (e.g., deafness, etc.), and a more abridged form for “bed¬ 
side histories,” which are of great convenience in cases of acute tympanic 
or mastoid disease. Copies of these two forms will be found in a final 
chapter or appendix. 

Objective Examination. — Before attempting to inspect the drum 
membrane by reflected light, much may be learned by a careful observ¬ 
ance of the patient. One may often determine at a glance whether the 
patient breathes normally— i.e., through the nose—or is a typical or partial 
mouth-breather. Habitual mouth-breathing in children is usually due to 
the presence of adenoids. This obstacle to normal breathing is, however, 



INSPECTION OF PATIENT 


43 


by no means invariably announced by the typically dull and vacant ex¬ 
pression so often described in the earlier text-books. The child is often 
of extremely healthy appearance. He may breathe quite normally during 
the day or when perfectly quiet, but with noticeable difficulty at night 
when the recumbent position favors nasopharyngeal congestion, or when 
engaged in any active physical exercise. While, therefore, we may often 
determine the presence of adenoids at a glance, our ability to do so can 
not be relied upon. Mouth-breathing in adults is less frequent, and usu¬ 
ally, therefore, more noticeable than in children. Whatever the patient’s 
age, habitual mouth-breathing should be noted as likely to throw light 
not only upon the etiology, but also upon the prognosis and treatment of 
the aural disease. 

In talking to a patient with advanced catarrhal deafness, one intui¬ 
tively gauges the degree of deafness by one’s difficulty in making him 
hear or by the evident difficulty on his part; also which is the deafer ear, 
by observing which ear is turned toward the speaker. By observing the 
patient’s expression and the intentness with which he scans the face of 
the person talking, one not infrequently discovers a capacity for lip- 
reading of which the patient himself may be only partly conscious. By 
such practical observations one may obtain very useful information as to 
the degree of deafness for which relief is sought. 

Auricular Displacement. —Of great importance, because of their 
possible surgical significance, are changes in the position of the auricle 
due to inflammatory processes in or about the ear. Note if the two auri¬ 
cles are identical in the angles which they form with the sides of head. 
While slight differences in this respect may represent simply an anatomical 
variation, marked differences are much more likely to be the result of an 
inflammatory condition in the ear or temporal bone of one or the other side. 
Marked projection outward and forward, or outward and downward, 
of one auricle beyond the position occupied by the opposite ear, points 
usually to an inflammatory process either in the mastoid cells (acute 
mastoiditis) or in the posterior wall of the fibrocartilaginous meatus 
(furunculosis). This outward displacement of the auricle is due either to 
a subperiosteal abscess or to oedema of the structures behind the ear,— 
i.e., those covering the mastoid process. The postauricular sulcus—linear 
depression between the auricle and side of the head—may therefore be 
obliterated. Such postauricular swelling, with outward displacement of 
the auricle, points in young children almost invariably to a suppurative 
inflammation involving the mastoid cells. In the adult, on the other hand, 
they may mean mastoid inflammation, with resulting subperiosteal ab¬ 
scess, but far more frequently are the result of an extension of inflammation 
from a furuncle in the posterior wall of the fibrocartilaginous meatus. 

Palpation in Case of Postauricular (Edema. —With oedema be¬ 
hind the auricle much may be learned as to the original focus of infection 
by careful palpation. Gradually exerted, but firm, pressure at a point 
upon the mastoid process just behind the auricular attachment, but so 


44 


EXAMINATION OF THE PATIENT 


directed as not to disturb the auricle, will elicit deep-seated bone tender¬ 
ness only if the mastoid process is the seat of an acute inflammatory 
process. If the mastoid is not involved, little or no pain will result from 
pressure so directed. On the other hand, pressure at exactly the same 
point, but directed slightly forward so as to move the auricle, will cause 
the patient to wince or cry with pain, even though the mastoid is perfectly 
healthy, if the fibrocartilaginous meatus be the seat of an acute inflam¬ 
mation. This latter phenomenon is, of course, explained by the fact that 
any movement of the auricle along the line of its attachment to the side 
of the head is necessarily communicated to the cartilaginous framework 
of the external auditory canal. It is a differential point of very consider¬ 
able diagnostic importance, and will be referred to again in a later chapter. 

Palpation of the Auricle in Case of Aural Pain. —Whenever ear 
pain is complained of, it is well to determine, if possible before any attempt 
is made to examine the drum membrane by reflected light, whether this 
pain is in any part due to an inflammation of the external canal. Except 
in infants and very young children, in whom the anatomical relation be¬ 
tween the drum membrane and external meatus is exceedingly close, manip¬ 
ulation of the auricle causes absolutely no pain when the inflammation is 
confined to the middle ear. On the other hand, very slight movements 
of the auricle are extremely painful even in the initial stages of a furuncle 
in the meatus. By pressing one’s finger firmly against the cheek immedi¬ 
ately above and in front of the auricle, and bringing it downward along 
the anterior attachment so as to press the tragus inward, one will elicit 
tenderness in every case in which the anterior wall of the meatus is the 
seat of an acute inflammation. If no pain.results from this procedure, 
the auricle should be moved in different directions,—upward, backward, 
downward, and forward. These movements will change the position of 
the different walls of the meatus, and if no pam is experienced one may 
with confidence exclude the fibrocartilaginous canal as the seat of an acute 
inflammation. 

If we have properly cultivated our powers of observation, we have 
now with the expenditure of but a few moments of time possessed our¬ 
selves of certain facts bearing upon the patient’s condition. We have 
made a piactical estimate of the degree of functional impairment (deaf¬ 
ness) by his difficulty in interpreting the conversational voice, have noted 
his capacity for lip-reading and the probable influence of this in supple¬ 
menting his power of audition, and have probably determined which is the 
deafer ear. If his disease is acute, we have either located the inflammation 
in the auricle or external auditory canal, or have excluded that part of 
the conducting mechanism as without bearing upon the aural disorder. 

The next step in the examination is the inspection of the drum 
membrane. For this purpose, the following mechanical aids are essential- 
(a) some form of artificial light, (b) a forehead mirror for focusing the light 
upon the membrana tympani, and (c) a properly constructed aural specu¬ 
lum. These appliances are found in the instrument houses in a variety 


THE FOREHEAD MIRROR 


45 


of designs. While some of them are excellent in every respect, others are 
so far from correct in design and structure as to be practically without 
value in aural work. It is important, therefore, that a brief statement be 
made as to the essential points which these instruments should possess. 

The Forehead Mirror .—In selecting a mirror for otological work, the 
points to be looked to are its size, the size of its central orifice, the position 
of the ball by which it is attached to the head-band, and, most important 
of all, its focal distance. Within certain limits, the size is a matter of 
personal preference, some instrument dealers showing them in various 
sizes from 2/ to 4 inches in diameter. In the writer’s experience, a mirror 
3 inches in diameter has represented the most satisfactory size. This 



throws a stronger light than those of smaller size, and, on the other hand, 
is lighter and less clumsy than larger ones. A 3%-inch mirror, however, 
if its attachment to the head-band is properly adjusted, can be used very 
satisfactorily and is the choice of many aurists. The central orifice should 
be not less than one-quarter of an inch in diameter, a smaller aperture 
entailing a certain amount of unnecessary eye-strain. The writer’s per¬ 
sonal preference is for a central orifice one-half inch in diameter, as shown 
in Fig. 38. This is particularly advantageous in tjunpanic surgery and in 
the post-operative treatment of mastoid wounds, a smaller aperture being 
apt to necessitate more frequent readjustments of the mirror, a serious 
inconvenience when one wishes to avoid touching anything not absolutely 
sterile. The ball by which the mirror is connected with the head-band 
should be attached to the peripheral edge (Fig. 38), rather than to its 



46 


EXAMINATION OF THE PATIENT 


posterior surface as shown by Fig. 39. The advantage of the peripheral 
attachment is that it allows a wider range of movement and also enables 
one to bring the central orifice nearer the eye. 

Undoubtedly the most important point to be investigated in select¬ 
ing a mirror for aural work is the focal distance. By this is meant the 
distance between the concave reflecting surface of the mirror and its 
principal focus, or that point in front of it at which the reflected rays con¬ 
verge to give the greatest brilliancy of illumination. It can be readily 
understood that a focal distance which would be quite satisfactory in 
examining the pharynx might be altogether unsuitable to the inspection of 



Fig. 40.—Head-banc! and mirror. 


so small a field as is afforded by the membrana tympani. Thus, a focal 
distance of 18 inches may afford a clear definition of the structures of the 
throat and pharynx, but would be altogether too great for the examination 
of structures so small as the minute landmarks of the drum membrane. 
For examining the ear, the focal distance should be not greater than 10 
or 12 inches. This may be easily tested by holding the mirror with its 
reflecting surface about twelve inches from the flame of a candle, lamp, or 
gas jet, and noting the distance at which the outline of the flame is most 
clearly shown upon any flat surface, c.^., a book-cover or the palm of 
the hand. This is also the point at which the convergent rays meet to 
give the most brilliant illumination. 



THE MIRROR AND HEAD-BAND 


47 


The Head-band. Of this but little need be said beyond the mention 
of certain points to be avoided. A head-band of any elastic material is 
unsuitable, because it allows a degree of motion which is precisely what one 
wishes to avoid. The flexible band should be made, therefore, of leather 
or of very stout silk ribbon at least an inch wide. The attachment of the 
mirror to the forehead piece should be effected by means of a double ball- 
and-socket joint, as shown by Fig. 40. A single joint does not allow of 
placing the mirror in the position which gives the least eye-strain and the 
clearest vision. Fig. 41 represents a stiff fibre head-band which’the writer 
has found very satisfactory in practical use. If properly fitted to the head, 
it is comfortable, and easily removed and put on. It has also the additional 



advantage over the ordinary head-band that it is more easily put on by an 
attendant or nurse during a surgical dressing, and usually falls automatically 
into its proper position on the head. 

To epitomize: If one were obliged to depend upon ordering a mirror 
and head-band by mail, one w^ould do well to include the following speci¬ 
fications: Diameter of mirror 3 to 3% inches; diameter of central orifice 
not less than one-quarter of an inch; attachment ball to be on the periph¬ 
eral edge of the mirror; focal distance 10 or 12 inches; head-band to be 
of stout unyielding material, and attachment mechanism to be provided 
with a double ball-and-socket joint. A mirror fulfilling these require¬ 
ments should prove quite satisfactory in otological work. 




48 


EXAMINATION OF THE PATIENT 



Fig. 42.—Aural specula. 




Fig. 44.—Tympanic probe. 



Fig. 45.—Aural cotton applicator. 











































AURAL SPECULA 


49 



Aural Specula (fig. 42). The accompanying illustrations represent 
some of the specula which are offered for sale, and with any of which the 
ear may be satisfactorily inspected by a competent aurist. In making 
one s choice one should bear in mind the mechanical results which the 
speculum is intended to facilitate. hat one needs is not a long and nar¬ 
row funnel which can be introduced deeply into the external auditory 
canal, but rather a short tube for introduction into the orifice of the fibro¬ 
cartilaginous meatus. Any unnecessary length of the tubular end of the 
speculum is a hindrance to inspection, and the facile use of instruments. 
The outer expanded portion of 
the speculum serves a double pur¬ 
pose,—viz. (1) that of a handle 
by which it is held in place and 
manipulated, and (2) that of a 
receptacle for collecting the light 
from one’s mirror and throwing 
it into the auditory canal. Any 
superfluous length of this portion 
of the speculum simply adds to 
the difficulties of inspection and 
local treatment of the ear. Asa 
teacher of practical otology, the 
author has been interested in ob¬ 
taining whatever speculum would 
best aid the medical student in 
acquiring quickly and easily a 
certain degree of facility in ex¬ 
amining the ear. He knows of 
no mere practical or satisfactory 
speculum than that shown in Fig. 

42, B, known as the Boucheron 
speculum. They are made in 
sets of four sizes. 

Three other instruments es¬ 
sential in aural examination are 
shown in the accompanying illus- Fiq - 46—Wall bracket for movable electric light. 

trations (Figs. 43, 44, and 45). 

The Source of Light. —Excellent light for otological work can be 
obtained from the flame of an oil lamp or gas jet, or from an electric bulb 
connected with the ordinary street current. Whatever the source may be, 
the light itself must be connected with some form of movable bracket 
which can be moved both in the vertical and horizontal planes (Fig. 40). 
The electric light is now quite generally used in the cities, and, when 
properly installed, gives a satisfactory and suitable form of illumination. 

Electric Forehead Lamp for Bedside Examinations .—Before leaving 
this subject, mention should be made of the lamp and pocket battery 


4 












50 


EXAMINATION OF THE PATIENT 


shown in Fig. 47. This little apparatus, which dispenses altogether with 
the mirror, has become an indispensable adjunct to one’s equipment for 
bedside examinations. The battery is supplied with six dry cells, which, 
unfortunately, must be renewed every four or five weeks. This, however, 
is a trifling disadvantage compared with the difficulties of inspection by 
other methods of illumination in private houses. 

Technic of Objective Examination; Landmarks of the Normal 
Drum Membrane. —Obviously our examination must be without value 
unless we have first prepared ourselves to recognize the physical charac¬ 
teristics of the normal ear. The student of otology will put his time to 
poor advantage unless his growth in technical skill and his knowledge of 

special anatomy are advanced 
simultaneously. The writer will, 
therefore, refer frequently to the 
anatomy of the parts under ex¬ 
amination. 

As with all kinds of work 
requiring technical skill, each in¬ 
dividual will inevitably in some 
degree develop his own method 
and technic. There are, however, 
certain points which the beginner 
will do well to bear in mind and 
adhere to strictly. 

Position of Physician and Pa¬ 
tient .-—For aural examination it 
is much better that the physician 
should be seated to one side of 
the patient (Fig. 48), rather than 
directly in front of him with 
knees parted. This brings his 
eye within easy visual range of 
the ear to be examined and is 
the most comfortable position 
To examine the opposite ear, 
it is easy to reverse this position either by revolving his own or the 
patient’s chair, or by rising and assuming the same position on the 
other side of the patient. 

Management of the Light .—The light should be about on the same 
horizontal plane as the patient’s ear, and so placed that the rays from it 
to the mirror and from the mirror to the ear shall be as nearly as possible 
parallel; i.e., they should form as acute an angle as possible. If the focal 
bistance of the mirror were exactly 10 inches, it would be better to bring 
doth the light and the ear under examination within that distance of the 
mirror. Usually, however, the focal distance is rather more than 12 
inches, so that the best illumination is obtained by placing the light be- 



Fig. 47.—Forehead lamp for bedside examination. 


both for him and for his patient. 







INSPECTION OF EAR 


51 



Fig. 48.—Position of physician and patient for aural examination 








52 


EXAMINATION OF THE PATIENT 


hind and to one side of the patient’s head, making the distance between 
the light and the mirror at least 18 inches. 




Fig. 49.—Section through adult canal and 
tympanum. 

I 



Fig. 51.—Diagram showing direction of audi¬ 
tory canal of adult. Dotted lines showing 
changed direction of canal by t raction upward. 


Fig. 50.—Section through canal and tympa¬ 
num of infant at term. 



Fig. 52. —Diagram showing direc-' 
tion of auditory canal of infant. 
Dotted line showing influence of 
traction downward upon calibre of 
canal. 


Use of the Mirror .—In inspecting so small a structure as the drum 
membrane by reflected light, one must necessarily use but one eye,— i.e. 
the eye behind the central orifice of the mirror. Both eyes, however, 
should be kept open, the habit, common to many beginners, of closing 














LANDMARKS OF THE NORMAL DRUM MEMBRANE 


53 


the opposite eye, causing a certain amount of unnecessary eye-strain. 
The mirror should be adjusted with the central orifice opposite the eye 
nearest the source of light. That is to say, if the light is placed to the 
patient’s left side, the mirror should be worn over the physician’s right 
eye, and vice versa. As inspection of the ear frequently occupies several 
minutes, and tympanic operations much longer, it is important that the 
physician’s body, head, and neck should be in a comfortable position. 
The light should, therefore, be thrown upon the ear and readjustments 
made altogether by movements and manipulations of the mirror,—the 
effort, common with beginners, to direct or adjust it by movements of 
the head usually resulting in very strained and uncomfortable positions 
of the neck. Having the light properly focused upon the ear, the student 
should devote some little time to holding it there steadily, inspecting 
carefully meanwhile the auricle and particularly the size and condition 
of the orifice of the meatus. He will make no satisfactory headway in 
the use of the speculum until he has the light under perfect control. 

Speculum Examination .—Before practising the use of the speculum, 
the student may refresh his memory of the anatomical differences between 
the external auditory meatus in the infant and that of the adult by ref¬ 
erence to the accompanying illustrations (49, 50, 51, 52). With adults 
it is often necessary to draw the pinna upward and backward in order to 
straighten the canal and bring the drum membrane into view. In the 
case of infants, on the other hand, one must usually draw the auricle 
somewhat downward and outward, in order to separate the floor of the 
canal from the roof and increase the angle between the drum membrane 
and the axis of the canal. 

As to the size of the speculum best suited to any particular case, one 
should select the largest that will enter the meatus easily and without 
force. Nothing is accomplished beyond discomfort to the patient by the 
attempt to use too large a speculum. The speculum is gently introduced 
into the meatus and carried beyond the hairs which occasionally obstruct 
its lumen near its external orifice. We may then examine the different 
walls of the meatus for signs of acute or chronic inflammation, and for 
the presence or absence of obstructing substances,— e.g., masses of ceru¬ 
men, foreign bodies, pus, serum, etc. The latter being absent, or having 
been removed, we may go on to the examination of the fundus of the 
canal,— i.e., the drum membrane (Fig. 53). 

Landmarks of the Normal Drum Membrane. —For the purposes of 
the present study, let us assume that we are to inspect a perfectly normal 
and healthy drum membrane. Letting the eye follow the roof or posterior 
wall to the fundus of the canal, one readily recognizes the membrane by 
the abrupt structural and color changes which distinguish it from the 
surrounding walls of the meatus. As seen by reflected light, it presents 
the appearance of a tense membrane stretched across the lumen of the 
inner extremity of the canal. It varies from bluish white to ivory white 
in color, having a peculiar sheen, or lustre, which is one of its most con¬ 
stant physical characteristics in health. While the color varies somewhat 


54 


EXAMINATION OF THE PATIENT 


within physiological limits in different individuals, loss of lustre invariably 
denotes either structural changes due to chronic disease, necrosis of the 
surface layer of epithelial cells resulting from acute myringitis, or the 
deposition of some foreign substance— e.g., mould (aspergilli), dried secre¬ 
tion, or powder blown into the canal—upon the drum membrane. The 
peripheral attachment to the tympanic ring (annulus tympanicus) is 
clearly outlined, showing the contour of the drum membrane to be irreg¬ 
ularly ovoid (Fig. 53). 

Toward the upper pole of the membrane, and nearer the anterior than 
the posterior margin, may be seen a small, projecting, glistening point, 
whiter than the surrounding structures,—usually described as of pin¬ 
head size, but in reality much smaller. Its appearance exactly portrays 
the actual condition,—that of a minute portion of the drum membrane 
pushed outward and forward into the lumen of the meatus by the small, 
projecting process of bone behind it,—the short process of the malleus 
(Fig. 53, c). This little structure, it will be remembered, lies almost in 




Fig. 53.—Normal drum membrane. 


the line of attachment of the anterior and posterior ligaments, or axis 
band, of the malleus, by which it is held firmly in position. It is the most 
constant landmark of the membrana tympani. It is found always in the 
upper and anterior part of the membrane, and is sometimes situated so 
far forward as to be apparently in contact with the annulus tympanicus. 

Scanning now the surface of the membrane, we discover the second 
landmark in a more or less prominent line running directly from the short 
process downward and backward toward the centre of the membrane. 
This is the manubrium mallei, or handle of the malleus (d). The hammer 
handle and short process are directly continuous one with the other. 
Hence each is the guide to the other. Thus, if the hammer handle is 
first located, by tracing it upward and forward we arrive at the short 
process; locating first the processus brevis, we trace the hammer handle 
by its invariable direction downward and backward from the short pro¬ 
cess toward the centre of the membrane. Until we have located one or 
the other of these landmarks, we can never be positive as to what part of 
the drum membrane we have in view,—nor in cases of middle-ear disease 
can we always determine with certainty whether it is the drum membrane. 











THE NORMAL DRUM MEMBRANE 


55 


Looking now at the lower and anterior part of the drum membrane, 
we*see a brilliantly shining triangular spot, the apex of which is located 
at the umbo, the opposite base being in the neighborhood of the lower 
and anterior arc of the tympanic ring. Its direction, therefore, from 
apex to base is downward and forward (e). This is spoken of as the cone 
of light, or light reflex, the latter term being not only descriptive but ex¬ 
planatory. It is due not to any structural change at this point, but simply 
to the fact that the tense membrane, drawn inward by the lower end of 
the hammer handle, falls normally throughout this triangular space into 
a plane perpendicular to the direction of the rays of light from the mirror, 
and, as this stream of light and the line of vision are coincident, the trian¬ 
gular light reflex results. Naturally, when the position of the drum mem¬ 
brane is changed in either direction,— i.e., is either bulging or retracted,— 
the cone of light is either altered or lost. Alterations or absence of this 
landmark are, therefore, indicative of displacement, but not necessarily 
of any structural change in the membrana tympani. 

Looking once more to the upper part of the drum membrane, we see 
passing almost horizontally backward from the short process a line or 
fold which is known as the posterior fold of the drum membrane (6). It is 
almost identical in position with the posterior ligament of the malleus 
which lies behind it. A shorter fold—so short in 
many cases as to be undemonstrable—runs for¬ 
ward from the short process to the anterior peri¬ 
pheral attachment of the drum membrane (b r ). 

It is called the anterior fold of the membrana 
tympani. Above these folds we may sometimes 
make out two very fine lines, running from the 
short process forward and upward, and upward 
and backward respectively (a, a'). These lines 
are known as the attachment strice of Prussak 
They pass from the short process of the malleus 
to the extremities of the original tympanic pro¬ 
cess or ring. Above these lines, and between them and that ungrooved 
part of the bony frame of the drum membrane which is formed by 
the outer plate of the squama, is a small space known as Prussak’s 
space. 1 It is identical in position with the Rivinian notch and is inclosed 
by ShrapnelFs membrane. 

Quadrants of the Drum Membrane (Fig. 54). — For convenience of 
description, the drum membrane is divided into four quadrants. If we 
imagine a vertical line passing directly downward from the umbo to the 
inferior margin, the drum membrane will be divided by this line and the 
hammer handle into two parts, an anterior and a posterior segment. Now, 
suppose another line, horizontal in direction, to pass through the umbo, 

1 Prussak’s space is so called because it marks upon the drum membrane the posi¬ 
tion of a small space within the middle ear called by the same name. (See description 
on page 25.) 



Fig. 54.—Diagram showing quad¬ 
rants of membrana tensa. 







56 


EXAMINATION OF THE PATIENT 


and the drum membrane is divided into four- quadrants,—viz., the pos- 
terosuperior (A), the posteroinferior (B), the anteroinferior (C), 'and 
the anterosuperior (D). 

The student or physician intending to practise otology, either as a 
specialty or in connection with other branches of medicine, should make 
himself thoroughly familiar, by examination of many ears, with the 
physical picture of the drum membrane as above drawn. At the same 
time he should bear in mind that what he sees is only part of the outer 
wall of the middle-ear cavity. Unless, therefore, he can supplement this 
picture by another, seen through the mind’s eye, of the structures behind 
the drum membrane, his examination is robbed of half its usefulness. He 
should know the position and relations of the different parts of the ossicular 
chain so thoroughly as to be unable to look at the drum membrane without 
subconsciously calling to mind the relations of the deeper structures 
within. In recalling these relations the student will perhaps be aided by 
reference to Fig. 55. In the vault are located the head of the malleus and 

body of the incus, the former an¬ 
teriorly and the latter posteriorly. 
In the atrium are found the short 
process and handle of the malleus, 
the long arm of the incus, and the 
whole of the stapes. Locating more 
exactly the parts of the ossicles in 
the atrium, we find in the antero¬ 
superior quadrant the short process 
of the malleus; in the posterosu- 
perior quadrant, the incudostapedial 
joint. Separating the anterosupe¬ 
rior from the posterosuperior quad¬ 
rant is the handle of the malleus. 
Behind the posteroinferior quadrant 
^ of the drum-head is the niche of 

riG. 55. — Semidiagrammatic picture, showing + • 1 rni • 

relations of ossicles in vault and atrium. Line A-B ^ lOUnU. WinuOW. I lie illiport- 

represents dividing line between atrium and vault, ance of fixing these points clearly 

and permanently in mind must 
be apparent. Of the four quadrants of the drum membrane the 
posterosuperior is the one which most insistently claims our attention in 
tympanic disease. In acute or chronic tubal catarrh retraction of this 
part of the drum membrane, by pressing upon the long arm of the incus, 
interferes in some degree with the movements of the incudostapedial 
joint, with consequent impairment of hearing. In hyperplastic or sclerotic 
processes involving the tympanum, the newly formed connective tissue in 
this region may reduce the mobility of the stapes and bring about very 
serious loss of function. In acute suppurative otitis media, also, the 
posterior segment of the drum membrane is commonly most noticeably 
in\ olved. It is in this region that incisions of the membrana tympani are 








DISPLACEMENT OF DRUM MEMBRANE 


57 


usually indicated. Obviously this operation, often so lightly undertaken 
and so imperfectly executed, is not without danger in unskilful hands. 

Having familiarized ourselves with its physical characteristics 'in 
health, we should now scrutinize each drum membrane examined for 
changes in color, position, or structure. 

Color .—To the practised eye even slight changes in color are not dif¬ 
ficult to recognize. Very considerable experience may, however, be re¬ 
quired to enable one to determine whether moderate redness is the result 
of temporary congestion or is due to a subacute inflammatory process with¬ 
in the tympanum. The interpretation of the commoner color changes will 
be spoken of in a later chapter dealing with the acute middle-ear diseases. 

Position .—While extreme displacement of the drum membrane in either 
direction is easily noted, slight changes from the normal position are quite 
difficult for the beginner to determine. Displacement outward, or bulg¬ 
ing, is usually accompanied by signs of acute inflammation, and is com¬ 
paratively easy to determine. The line of attachment of the hammer 
handle may be rendered indistinct or be completely lost to view as a result 




Fig. 56.—Bulging drum membrane. 


of inflammatory thickening or infiltration of the drum membrane. The 
bulging portion of the drum membrane balloons outward into the lumen 
of the canal and appears nearer the examiner’s eye, as it really is, than the 
peripheral portions (Fig. 56). 

Displacement of the drum membrane inward, or retraction, is com¬ 
monly unaccompanied by any of the signs of acute inflammation. The 
membrana tensa, carrying with it the hammer handle, is moved inward 
toward the promontory. The drum membrane, in being drawn or forced 
inward, folds itself about, or tends to form angles with, the structures to 
which it is attached. Hence the short process, the foreshortened hammer 
handle, the anterior and posterior folds, and in some cases the annulus 
tympanicus may appear unduly prominent (Fig. 57). While extreme 
retraction is easily made out even by the beginner, it requires consider¬ 
able practice and experience to determine slight departures from the 
normal in this direction. The characteristic signs of moderate retraction 
will be described under tubal catarrh. 

Structural Changes .—Changes in structure may take the form of uni- 










58 


EXAMINATION OF THE PATIENT 


form or localized thickening, of moderate or extreme atrophy of the drum 
membrane, of cicatrices due to old perforations, or of actual loss of con¬ 
tinuity,— i.e., perforations,—which may vary in size from a small pin¬ 
head orifice to practical destruction of the membrana tensa. Localized 
thickening of the drum membrane is shown usually by areas of opacity. 
Such opaque spots are not infrequently seen in the drum membranes ol 
individuals whose hearing is not noticeably impaired, and are supposed in 
some cases to be due to calcareous deposits representing one of the tissue 
changes resulting from the rheumatic, or uric acid, diathesis. 

Atrophy, either general or localized, is shown in some cases by abnormal 
thinness and transparency of the membrana tensa. In others the atrophic 
area appears opaque and thicker than the rest of the membrane. The 
latter condition represents an increase in connective tissue at the expense 
of the fibrous layer of the drum membrane. In such a case the atrophy is 
revealed only by the abnormal relaxation, or loss of tension, in the areas 
involved, as shown by Siegel’s pneumatic otoscope to be described presently. 

Perforations of the drum membrane are best observed by mapping 
out as nearly as possible the limits of the membrane by its peripheral 
attachment to the annulus t} r mpanicus, and then looking closely for any 

loss of continuity in its surface within this space. As the 
line of demarcation between the roof of the meatus and 
Shrapnell’s membrane is sometimes obliterated bj r inflam¬ 
matory thickening or infiltration at this point, it is well 
to begin by letting one’s glance travel inward over the 
roof of the canal and follow the drum membrane down¬ 
ward to its inferior margin. When the margins of a per¬ 
foration are clearly defined and there is an appreciable 
space between the membrane and the inner tympanic wall, the form 
and extent of the perforation are easily determined. On the other hand, 
with a swollen tympanic mucosa in contact with a small and ill-defined 
perforation, its detection may present great difficulties to the beginner. 

A perforation having been made out, its exact position should next 
be observed, and this can be determined positively only by noting its 
relation to either the short process or handle of the malleus. For example, 
a perforation behind the hammer handle must be in the posterosuperior 
quadrant. The student will do well to acquire early the habit of drawing 
diagrams of the drum membrane and noting thereon the morbid changes 
observed. The accompanying diagram (Fig. 58), made with a few strokes 
of the pen, indicates more clearly the exact size, form, and location of the 
perforation than could any amount of descriptive written matter. 

Variations in Tension .—Conditions which cannot be determined by 
inspection alone are general loss of tension, relaxation of certain portions 
of the membrane, adhesions between the membrane and the inner tym¬ 
panic wall, fixation of the hammer handle to the promontory, etc. To 
investigate these conditions one must depend upon some apparatus which, 
while leaving the drum membrane in clear view, produces alternate con- 



Fig. 58.—Rough 
pen-and-ink dia¬ 
gram of the drum 
membrane. 


VARIATIONS IN TENSION 


59 


densation and rarefaction of the air in the external auditory meatus. 
The Siegel otoscope (Fig. 59) admirably fulfils this need. 

It consists essentially of a speculum (a), the expanded end of which 
is closed by a thin plate of glass through which the movements of the 
drum-head may be observed. Communicating with its interior bv an 
aperture in the side of the speculum is a short rubber tube (6) the other 
end of which is connected with a Delstanche pump or, better, with a 
rubber bulb (c). With the small end of the speculum moistened and 
introduced into the auditory canal, the interior of the speculum and of 
the auditory meatus form practically an air-tight compartment. When 
the bulb is compressed, the air in the external auditory canal is condensed 
and the drum-head is forced inward; when pressure upon the bulb is 


Fig. 59.—Siegel’s otoscope. 



released, the air in the meatus is rarefied and the drum membrane is 
sucked outward into the canal. Using the Delstanche pump, we produce 
the same mechanical results by moving the piston alternately toward and 
from the drum membrane. Under these manipulations the normal drum¬ 
head moves fairly evenly, the posterior segment on account of its larger 
surface moving rather more than the anterior. In these movements the 
hammer handle participates, though its excursions are less extensive and 
more difficult to follow with the eye than those of the posterior segment 
of the drum membrane. 

Obviously the use of this instrument is advisable and of value only 
in chronic disease of the tympanum. It is equally clear that the move¬ 
ments of the diseased drum membrane might differ greatly from those 
characteristic of health, and might throw very considerable light upon 
the lesion with which the physician has to deal. Thus, a generally relaxed 



















60 EXAMINATION OF THE PATIENT 

drum membrane would execute exaggerated movements both in the an¬ 
terior and posterior segments, these movement having relatively small 
influence upon the hammer handle. Atrophy or loss of tension, localized 
in certain portions of the drum membrane, would be evidenced by the 
ballooning of these sections, independently of the rest of the membrane, 
outward into the meatus. Adhesions of the drum membrane to the prom¬ 
ontory or to any structures within the tympanum would be clearly dem¬ 
onstrated by its fixation at those points. 

Examination of the Eustachian Tubes.—In all cases of chronic aural 
disease the condition, of the Eustachian tubes must be determined be¬ 
fore a correct diagnosis can be made. Inflation of the tympanum, which 
throws light both on the patency of the tubes and the condition of the 
middle ear, is therefore an essential part of the aural examination in a 
large class of cases. There are three recognized methods of inflation,— 
viz. (1) Valsalva’s method , (2) Politzer’s method , and (3) inflation by means 
of the Eustachian catheter. 

Valsalva’s method of inflation has a very limited field of useful¬ 
ness. It is performed when the patient, with lips tightly closed and nostrils 
occluded by compression of the nose, attempts forcible expiration. By 
this procedure the air in the nasopharynx is condensed and finds its way 
under pressure through the Eustachian canals to the middle-ear cavities. 
This normally requires little effort, but naturally calls for greater force if 
the calibre of the tubes is reduced, or if the pharyngeal orifice of either 
tube is occluded by localized swelling or congestion in that region. It is 
a measure of which little use is made in otology. Patients, however, often 
intuitively acquire the habit of inflating the ears in this way as a means 
of relieving the discomfort arising from tubal catarrh, and when this is 
made known to us we may safely conclude that the function of the Eusta¬ 
chian tubes is disturbed. We may also in such cases draw conclusions as 
to which tube is the more occluded by requiring the patient to repeat 
the act and to note which ear is first inflated,—the ear last inflated cor¬ 
responding, of course, to the more obstructed tube. If this ear is also the 
one in which the subjective symptoms are most marked, we have already 
some data upon which to base an opinion. Personally the author makes use 
of the Valsalva method of inflation in the diagnosis of one condition only, 
—viz., cases in which one may suspect the existence of a small perforation 
in the drum membrane which can not be determined definitely by inspec¬ 
tion alone. In such a case if the patient be required to force air into the 

tympanum while the drum membrane is kept under view, a drop of fluid_ 

serum or pus—will appear at the point of the perforation, or a more or 
less shrill whistle will result from the passage of air through the small 
opening in the membrane. If the drum membrane balloons outward into 
the lumen of the meatus without the appearance of either of these phenom¬ 
ena, it may be confidently assumed that no perforation exists. This, in 
the writer’s opinion, is the one condition in which the Valsalva method is 
of real diagnostic value. That is to say, there is no other condition in 


POLITZER’S METHOD OF INFLATION Cl 

I 

v Inch 8.11 that may be learned, from Valsalva inflation may not be better 
obtained in some other way. It is a measure which may easily become a 
habit with the patient to the detriment of the ear, and its general or 
frequent use is to be advised against. 

Politzer’s method of inflation resembles that of Valsalva in that 
both depend upon condensation of the air in the nasopharynx. Since 
this procedure was first proposed, the universal recognition of its value 
and its general adoption by otologists of all countries have resulted in 
some slight modifications in the instruments employed. 

Politzer’s inflating apparatus (Fig. 60) consists of a compressible, 
soft rubber air-bag communicating at one end with a piece of rubber tub¬ 
ing the end of which fits over a hard rubber tubular nozzle, or nose-piece. 



The air-bag is provided with a valve by means of which, after the contained 
air has been expelled, a fresh supply is taken in without the necessity of 
removing the nozzle from the patient’s nose. 

Technic .—The patient and physician are seated opposite each other. 
The former is given a glass of water and told to take a sip of it into his 
mouth and to swallow it at a signal from the physician. With his left 
hand the physician now inserts the nozzle of the inflating apparatus into 
the patient’s nostril corresponding to the ear he wishes to examine, at 
the same time closing the nasal passages by pressure upon both alee nasi. 
The air-bag meanwhile is held ready for use in the physician’s right hand. 
The patient is now told to swallow and, synchronously with this act on 
his part, the air-bag is quickly and forcibly compressed. The act of deglu¬ 
tition brings the soft palate into contact with the posterior wall of the 
pharynx and effectually closes the nasopharynx. The air in the naso- 









62 


EXAMINATION OF THE PATIENT 


pharynx is at the same time condensed by the influx of additional air from 
the inflating bag, and forces its way through the Eustachian tubes into the 

tympanic cavities. By reason of the valvular 
opening in the air-bag, inflation by this method 
may be repeated several times without removing 
the end-piece from the patient’s nose. A 
modification of Politzer’s method is by requir¬ 
ing the patient, instead of swallowing water, 
to repeat some word ending in K,—thus, hock, 
hock, hock, etc.,—the lingering enunciation of 
this guttural as a terminal sound serving to 
hold the soft palate in contact with the pos¬ 
terior pharyngeal wall and thus shut off the 
nasopharynx from the laryngopharynx below. 
The first method, however, has the advantage 
that the act of swallowing not only closes 
the nasopharynx but also serves to separate 
the anterior from the posterior wall of the 
membrano-cartilaginous tube, and thus facili¬ 
tates the freer passage of air to the tympanum. 
Another method is by requiring the patient, 
after the tip of the inflating apparatus has 
been properly adjusted, to close the lips 
tightly and forcibly balloon out the cheeks. 
This, of course, does not close the nasopharynx, 
but serves to condense the air in the entire 
respiratory tract. Obviously the pressure of 
additional air from the air-bag would tend to 
force the patency of the tubes. It seems to be 
a combination of the Valsalva and Politzer 
methods. It is very useful in dealing with cer¬ 
tain children who will not co-operate with the 
physician in carrying out the method as proposed 
by Politzer. 

Politzer’s method of inflation has a wide field 
of usefulness. As a diagnostic measure its posi¬ 
tion is distinctly secondary to inflation by cathe¬ 
ter. It must be used, however, in certain classes 
of cases, among which are the following: 

(1) Young children, who will rarely submit to 
catheterization. 

(2) Very nervous adults who in some cases 
(rare) will not submit to the use of the catheter 
at the first sitting. 

(3) Adult patients in whom nasal abnormalities or occlusions contra¬ 
indicate or render impossible the use of the catheter (rare). 



Fig. 61. —Eustachian catheter 
(silver). 










INFLATION BY CATHETER 


63 


Inflation per Catheter. —In the writer’s opinion the catheter offers 
by far the most satisfactory and reliable method of examination in the 
great majority of cases. Its full usefulness, however, requires a degree of 
technical skill and experience in interpreting the sounds heard through 
the otoscope, which can be acquired only after long practice. The student 
of practical otology can not, therefore, too carefully or persistently practise 
its use. If at the end of a year’s practice in a busy clinic he has acquired 
considerable skill in catheterization, he will assuredly be yet more skilful 
at the end of a second year. By skill is meant not merely the ability to 
find the tubal orifice, but to accomplish this with the least mechanical 
irritation of the nasal and pharyngeal mucosa, and therefore with minimum 
injury and discomfort to the patient. As it is absolutely essential that the 
necessary instruments be of right material and design, a few words may 
well be devoted to them here. 

The Catheter .—The accompanying figure (Fig. 61) clearly illustrates 
the correct size and form. The expanded outer end (a) receives the tip or 
end-piece of the inflating apparatus. The small end (6) must be smooth, 
— i.e.j without sharp edges which might injure the nasal or tubal mucosa. 
The curve near the end enables the physician, after it has passed into the 
cavity of the nasopharynx, by rotating the catheter, to bring the beak 
into the Eustachian orifice. While the curve indicated in the illustration 
is the one best suited to a majority of cases, it obviously must be changed 
somewhat to meet the anatomical requirements of certain pharynges. 
The catheter should therefore be made of malleable silver to allow of such 
changes as may be required. The ring (c) is of use as a guide by which in a 
case presenting anatomical difficulties the surgeon may know in what 
direction the beak is pointing. As to length, the writer uses and prefers 
a catheter of 5% inches. It should not exceed 6 inches. Any unnecessary 
length— i.e., which leaves more of the catheter outside of the nose than is 
necessary for its manipulation—simply interferes with its proper control 
and adds to the patient’s discomfort. A catheter longer than 6 inches has 
never in the writer’s experience been found necessary. Ihe catheters 
come in three sizes, or calibres, of which the illustration represents the 
intermediate, and the one indicated in the great majority of cases. The 
largest is practically never used by the writer. The smallest is necessary 

in some cases. 2 

The Dench inflating apparatus (Fig. 62) is undoubtedly the best so 
far devised for catheter inflation. Between the air-bag (a) and the tip (c) 
which fits into the outer end of the catheter, is a hard-rubber bottle ( b ). 
This bottle enables one to employ medicated vapors in the treatment of 
the tubal and tympanic mucosa. When the stopper is in the position 

2 Catheters of hard rubber, described in some text-books, are to be condemned, if 
for no other reason, because they can not be thoroughly sterilized Catheters of hard 
‘‘German silver” offer the decided disadvantage that they can not be bent Catheters 
with bulbous ends do not admit of as fine adjustment as those of smaller terminal 
calibre, but may offer distinct advantages as practice instruments lor beginners. 






EXAMINATION OF THE PATIENT 


64 

shown in the illustration (d-e), air expelled from the air-bag does not pass 
through the bottle and is therefore not influenced by its contents; but 
when the stopper is turned so as to occupy the position indicated by the 
line f-g, the air must pass through the bottle before reaching the catheter 
and is in this way impregnated with any volatile drugs— e.g., alcohol, 





solutions of menthol, camphor, iodine, etc.—therein contained. The 
rubber tubing prevents the movements of the air-bag from being commu¬ 
nicated to the catheter. The valvular opening into the air-bag enables the 
physician to repeat the act of inflation any number of times without 
moving the catheter. 

The Otoscope or Diagnostic Tube (Fig. 63). —This is simply a piece of 
rubber tubing, about 30 inches long, into each end of which is fitted a 
small hollow ear-piece somewhat similar to, but smaller than, the ear-tips 



of the ordinary stethoscope. Usually one is of white bone and the other 
of hard black rubber. This enables one to distinguish them,—an obvious 
advantage in a busy clinic, where the aurist may be pardoned for wishing 
to reserve one end for himself, leaving to his patients the exclusive use of 
the other. Inserting one end into his own ear and the other into that of 
his patient, he can during inflation obtain fairly accurate information as 






























DIAGNOSTIC VALUE OF OTOSCOPE 


65 


to the condition of the tube and tympanum by the auscultatory signs 
obtained through the otoscope. With a normal tube and tympanum, he 
will hear during inflation a rather low, blowing sound giving somewhat 
the impression of a sound originating in his own ear. While usually low, 
the pitch will of course vary somewhat with variations in the calibre of 
different tubes. 

Of abnormal conditions which may be made known to us by the oto¬ 
scope, may be mentioned the following: 

(a) Absolute occlusion of the tube as shown by absence of all sound of 
air entering the tympanum. Obviously this sign is without value unless 
the physician has sufficient technical skill to feel sure that his catheter is 
properly placed. 

(b) Patent but abnormally narrow tube, shown by clear sound of unusu¬ 
ally high pitch. 

(c) Abnormally wide tube, made known by very low-pitched, rough 
sound and the absence of any resistance to the compression of the air- 

bulb. 

(d) Presence of excessive mucus or other fluid secretion within the tube, 
shown by small, intermittent rales, finally ceasing as the moisture is dis¬ 
tributed or blown into the nasopharynx by the return air current. 

(e) Presence of fluid in atrium, shown by more or less constant, bub¬ 
bling rales, giving the impression of air passing through fluid,—the actual 
physical condition. 

(f) Abnormal relaxation of the drum membrane, as shown by certain 
characteristic sounds due to the flapping outward of the drum membrane 
during compression of the air-bag, and its recoil as the air pressure 
subsides. 

(g) Small perforations of the drum membrane, made known by whistling, 
squeaking, or singing sounds due to vibration of the edges of the perforation. 

(h) Large perforations in, or absence of, the drum membrane, made 
known by the sensation of air blowing against the physician’s drum 
membrane. 

It is quite useless to attempt to describe more minutely than as given 
above the various sounds and signs obtained through the otoscope during 
inflation. With practice and careful study of cases, these sounds will 
soon rank among the most valuable guides as to the conditions present. 

Technic. —The physician is seated directly opposite his patient, with 
the ends of the diagnostic tube adjusted in his own and the ear to be 
inflated (Fig. 64). The patient is directed to hold the head with chin 
slightly depressed, to keep the mouth closed, to continue breathing quietly 
through the nose, and to resist the impulse to jerk or move the head back¬ 
ward and out of the physician’s reach. He is asked to hold the bottle of 
the inflating apparatus, this arrangement leaving the air-bag in convenient 
reach of the physician’s hand. To be in proper relation to the mouth of 
the tube, the catheter must reach the nasopharynx by way of the inferior 
meatus of the nostril corresponding to the ear to be inflated (ligs. 65 and 
5 


66 


EXAMINATION OF THE PATIENT 



Fig. 64. Position of physician and patient during 


catheter inflation 









TECHNIC OF CATHETER INFLATION 


67 


66). At the start the catheter is held between the thumb and forefinger of 
the right hand, the tip of the inflating apparatus being held between the 
third and little fingers of the same hand, ready for introduction into the 
outer expanded end of the catheter as soon as the latter shall have been 
placed in proper position. Holding the catheter at first almost in the 
vertical position, with the curved end pointing forward, the tip is intro¬ 
duced into the inferior meatus of the nostril corresponding to the ear to be 
inflated. In order to insure against its entering the middle meatus, it is 
now quickly elevated from the vertical into the horizontal position as it 
enters the nostril, the tip being kept in light contact with the nasal floor, 
and is carried directly backward until it is felt in very light contact with 
the posterior pharyngeal wall. It is next rotated outward toward the ear 
until the guide ring points in a direction about midway between the hori¬ 
zontal and vertical planes. It is then withdrawn slightly until its beak 
is arrested by the anterior wall of the fossa of Rosenmiiller, which, it will 
be remembered, corresponds in position with the posterior wall of the 
Eustachian orifice. Over this elevation it is now lightly drawn, the cathe¬ 
ter being then rotated further outward and upward until the guide ring 
points somewhat upward, describing an angle of 30 or 35 degrees with the 
horizontal plane. This should bring its extremity into its proper position 
in the pharyngeal mouth of the tube. The outer end of the catheter is 
now transferred to the left hand and the tip of the inflating tube carefully 
inserted. 3 The right hand is thus free to grasp the air-bag, and the difficult 
part of the procedure is accomplished. The sounds heard through the 
otoscope now furnish additional information as to the exact position of 
the catheter within the Eustachian orifice, and enable one to make such 
slight readj ustments as are necessary to give the best inflation. 

Other methods of placing the catheter have been described,—as, 
for instance, (1) by passing the catheter as before, through the inferior 
meatus until its beak touches the posterior wall of the pharynx, rotating 
it toward the opposite ear, withdrawing it until its curved end is engaged 
by the posterior margin of the nasal septum, then rotating it downward 
and outward in the opposite direction until its beak enters the Eustachian 
orifice; (2) passing the catheter backward with beak resting on the nasal 
floor, noting when the beak sinks into the nasopharynx and then rotating 
it directly into the orifice of the tube to be inflated. These are distinctly 
less reliable than the method first described, which is the one which should 
be practised by the student of practical otology. By so doing he will 
surely in time acquire a facility which will enable him to dispense with 


3 Some aurists prefer and advise that the tip of the inflating apparatus should be 
securely inserted into the outer end of the catheter before the latter is introduced into 
the patient’s nose. This prevents the discomfort which might arise during its adjust¬ 
ment after the catheter is in position. In the writer’s experience a more delicate manip¬ 
ulation of the catheter has seemed possible by the method above advised. A little 
practice will enable one to make the connection between the catheter and the inflating 
apparatus without discomfort to the patient. 



68 


EXAMINATION OF THE PATIENT 


some of the steps described. Thus, the practised aurist learns to ignore 
the fossa of Rosenmiiller as a guide, and intuitively withdraws the catheter 
to the right position opposite the mouth of the tube. The student, however, 
will do well to follow literally the steps here described, which alone will 
lead to the degree of technical skill which robs this procedure of its 
discomfort to the patient. 



Fig. 65. —Correct pathway of catheter to posterior pharyngeal wall. 

Fig. 66. —Correct position of catheter within tubal orifice. 

Fig. 67. —Incorrect introduction of catheter,— i.e., through middle meatus. 


There are one or two points mention of which may be of use to the 
beginner. He should learn at the start to recognize surely the sound 
which comes to him through the otoscope when the end of the catheter 
is not in the mouth of the tube but in the fossa of Rosenmiiller. This 
sound is loud, rough, does not have the character produced by air passing 
through an open tube, and does not sound as if originating in or near the 
physician’s own ear. Unless this sound is definitely recognized, the stu¬ 
dent may waste considerable time in the mistaken belief that he is prac- 






















Plate IV 



Fig. 68.—Tongue depressor (A). Fig. 70.—Nasal speculum (C). Fig. 72.—Cotton applicator (E) 

Fig. 69.—Nasal speculum (B). Fig. 71.—Laryngeal mirror (D). Fig. 73.—Nasal probe (F). 


















SURGICAL EMPHYSEMA 


69 


tising inflation while in reality his catheter may never have entered the 
Eustachian orifice. When properly placed, the catheter is held in position 
by slight pressure of the outer end against the nasal septum, this tending 
to throw the other end, or beak, in the opposite direction and further into 
the Eustachian orifice. If now the patient complains or shows signs of 
pain, learn from him whether the pain is referred to the nose or the throat. 
If in the nose, slight shifting of the position of the catheter here or easing 
of the pressure will usually relieve the discomfort. If, however, the pain 
is referred to the throat, it is due often to rotation of the catheter too far 
in one or the other direction. A little care in correcting these minor errors 
of technic will render this a bearable, if never a pleasant, experience to the 
patient. 

Surgical Emphysema— There is one accident which must be mentioned 
as a possible result of careless catheter inflation,—viz., traumatic emphy¬ 
sema. It occurs when air from the inflating apparatus is propelled through 
some false passage into the tissues surrounding the membrano-cartilaginous 
tube. It probably always indicates either an abrasion of the tubal mucosa, 
or an incorrect position of the catheter, as a result of which air is forced 
through the mucous membrane into the tissues beneath. The accident 
usually gives rise to very sharp and sudden pain, which is, therefore, an 
indication that the inflation should be immediately discontinued. The 
diagnosis is confirmed when palpation of the tubal region—he., between 
the tip of the mastoid and the angle of the jaw and downward along the 
anterior border of the sternomastoid—is accompanied by distinct crepitus. 
While painful and often alarming to the patient, the condition is not dan¬ 
gerous, the air being usually absorbed within from 24 to 48 hours. The 
patient should, therefore, be assured that the symptoms will disappear 
spontaneously within a day or two. If treatment is called for, very gentle 
massage may help to expel the air from the tissues. 

The Nose, Nasopharynx, and Throat. — The relation of the ear to 
the nose and nasopharynx is so intimate, and the diseases of the two 
regions are so interdependent, that one must assume for the special stu¬ 
dent of otology some preliminary or collateral study of rhinology and 
laryngology. No examination of the ear is complete until one has care¬ 
fully inspected the nose and nasopharynx. The author will speak very 
briefly of this region, dealing only with what he believes to be absolutely 
essential to a complete aural examination. 

A forehead mirror with focal distance of from 12 to 15 inches gives very 
satisfactory illumination. In addition to the mirror, the instruments 
necessary in an examination of the nose and pharynx are a tongue depressor 
(Fig. 68), a nasal speculum (Figs. 69, 70), a postnasal mirror (Fig. 71), 
cotton applicators (Fig. 72), and a nasal probe (Fig. 73). 

One saves time by observing some regular order in one’s examination, 
and the author prefers to examine first the nasal cavities, then the posterior 
wall of the pharynx and the faucial tonsils, and last the nasopharynx, or 
postnasal space. 


70 


EXAMINATION OF THE PATIENT 


Examination of the Nose. —From the view-point of the aurist the 
examination of the nose is chiefly for the purpose of determining any 
condition within the nasal cavities which may predispose to, or directly 
excite, nasopharyngeal congestion and catarrh of the Eustachian tubes. 

The conditions to be looked for are: (1) Abnormalities of the nasal 
septum, — e.g. (a) deflections to one or the other side. This may be very 
slight or so marked as completely to occlude one nostril. It may be 
limited to the anterior cartilaginous portion, or include the posterior or 
osseous part of the septum, involving the vertical plates of both the vomer 
and ethmoid, (b) Localized septal ridges or spurs, which again may be 
confined to the cartilaginous part (ecchondroses) or to the posterior bony 
portion (exostoses), or the ridge may include both, running from before 
backward and upward along the line of junction of the vomer to the cartilage 
in front and to the ethmoid plate behind. (2) Hypertrophy of the turbi¬ 
nated bodies. By anterior rhinoscopy one can usually see only the anterior 
half of these structures. If one or both inferior turbinates are noticeably 
enlarged, we should determine by palpation whether the increase in size is 
due to an actual hyperplasia— i.e., depositions of new connective tissue— 
or to engorgement of the turbinal vessels. In the former case the turbinal 
body offers considerable resistance to compression by means of the nasal 
probe, and its size is only moderately reduced by the application of adren¬ 
alin or cocaine. When the enlargement is due to vascular engorgement, 
the turbinate pits deeply on pressure but quickly regains its former size 
as soon as the compressing probe is removed, and it shrinks enormously 
under the influence of the suprarenal preparations. 

The middle turbinates are not quite so easily inspected. When the 
septum is deflected to one or the other side, it may be quite impossible to 
see the middle turbinate on the side to which the septum is bent, without 
first shrinking the corresponding inferior turbinal body. Usually, however, 
by means of a proper speculum and by tilting the patient’s head somewhat 
backward, both middle turbinates may be brought into view. Whenever 
either of these bodies are noticeably enlarged, the corresponding nasal 
cavity should be thoroughly exsanguinated by means of adrenalin chloride. 
This aids in determining to what extent, if any, the enlargement is due to 
simple congestion. The nasal cavity should now be carefully inspected 
for nasal polypi and for a possible escape of pus from the middle meatus, 
— i.e., from beneath the middle turbinate. Either of these conditions 
might point to disease involving either the frontal sinus or the anterior 
ethmoid cells, or both. 

The Throat. In examining the throat, one should endeavor to train 
one’s eye to observe quickly, prolonged use of the tongue-depressor caus¬ 
ing discomfort, reflex pharyngeal irritation, and often retching. This may 
render subsequent examination of the postnasal space unsatisfactory or 
impossible. The tongue-depressor should be introduced into the mouth 
only so far as is necessary to press upon the most elevated and arched 
portion of the dorsum of the tongue,—pressure too far back causing re- 


POSTERIOR RHINOSCOPY 


71 


flex irritation and “gagging/' or retching. With the tongue depressed, 
one should note quickly first the size of the faucial tonsils,— i.e., whether 
they'are of normal size or hypertrophied. As to the standard by which 
the size is to be judged, so distinguished an authority as Bosworth is of 
the opinion that whenever the tonsil is demonstrable by inspection, it 
should be regarded as representing an abnormal growth. The more com¬ 
monly accepted view is that any projection of the tonsil toward the median 
line so as to encroach, however slightly, upon the cavity of the pharynx 
is abnormal, and represents hypertrophy. It must be remembered that 
tonsils but slightly enlarged while the patient is in his usual health may be 
subject to great increase in size under the influence of any nasopharyngeal 
congestion or inflammation,— e.g., a common “cold.” Moderate hyper¬ 
trophy of the tonsils in adults may, however, be absolutely without in¬ 
fluence upon the ears. In young children, on the other hand, any consid¬ 
erable enlargement of the faucial tonsils is almost invariably associated 
with the presence of pharyngeal adenoids. Tonsillar hypertrophy has, 
therefore, a very decided bearing upon the condition of the ears in 
childhood. 

On the posterior pharyngeal wall one should note the presence or 
absence of the following conditions,—viz.: (a) Dilatation of the superficial 
veins, a condition which in adults very frequently results from nasal 
obstruction and the irritation due to mouth-breathing during sleep, (b) 
The so-called granular pharynx, characterized by the presence of granula¬ 
tions upon the pharyngeal wall. They are usually most noticeable along 
the median line of the pharynx just behind and below the uvula. This 
condition in children almost invariably indicates the presence of naso¬ 
pharyngeal adenoids, (c) The presence of dried or tenacious secretion 
adhering to the pharyngeal wall. With this is frequently seen a more or 
less glazed condition of the pharyngeal mucosa, a condition characteristic 
of atrophic rhinopharyngitis, (d) The physical signs of acute pharyngitis. 

Posterior Rhinoscopy. —The examination of the postnasal space by 
means of the small rhinoscopic mirror forms an important part of the 
examination of adult patients suffering from aural disease. It consists of 
depressing the tongue by means of a tongue-depressor, and inserting a 
small mirror backward over the tongue, under and behind the soft palate, 
so that by reflected light one may obtain a clear view of the roof of the 
pharvnx, the posterior margin of the nasal septum, the posterior ends of 
the middle and inferior turbinal bodies, the fossae of Rosenmuller, and the 
pharyngeal orifices of the Eustachian tubes. Here, even more than in 
examining the posterior pharyngeal wall and faucial tonsils, it is impoi tant 
to acquire the habit of quick but accurate observation. Of possible abnor¬ 
malities bearing upon an existing aural disorder, one should look especially 
for the following conditions,—viz.: (A) Hypertrophied lymphoid tissue 
upon the roof of the nasopharynx . An adenoid growth in this region, if 
of considerable size and located well forward, will inevitably cut off from 
view the upper part of the nasal septum. If the whole of the posterior 


72 


EXAMINATION OF THE PATIENT 


margin of the septum can be seen, and the roof of the pharynx arches 
evenly above this without noticeable obstructing mass, the cause of an 
existing nasal or aural disorder must be looked for elsewhere. (B) Lym¬ 
phoid hypertrophy in the fossoe of Rosenmuller. In some cases—and par¬ 
ticularly where previous operations for the removal of adenoids have 
been performed—the pharyngeal roof may be practically clear yet con¬ 
siderable masses of adenoid tissue are found behind the Eustachian ori¬ 
fices in the fossae of Rosenmuller. This condition is particularly likely to 
induce morbid changes in the middle ear, leading to permanent impair¬ 
ment of hearing. (C) Hypertrophy of the posterior ends of the inferior 
turhinal bodies. This condition is nearly always dependent upon some other 
lesion in the anterior nares. (D) Congestion , or swelling , of the tissues about 
the Eustachian tubes. This is often quite noticeably present during acute 
tubal catarrh, and is usually dependent upon some coexisting nasal or 
nasopharyngeal lesion. 

Any of the above conditions would necessarily have some bearing 
upon an aural disorder. Their presence or absence is best determined in 
adult patients by posterior rhinoscopy. With young children, on the other 
hand, the use of the postnasal mirror is in most cases impossible, and we 
are obliged to depend upon digital examination. The technic of examin¬ 
ing the postnasal space by reflected light has been so fully described in 
most text-books on diseases of the throat and nose, that its repetition 
here hardly seems necessary. 4 Inspection of this part of the respiratory 
tract forms, however, a very important part of every aural examination 
in adults, and should be carefully practised by every aurist who would do 
thorough and effective work. 

Obviously there are many cases—including all cases of non-suppura- 
tive aural disease—in which the examination would be altogether unsatis¬ 
factory without careful testing .of the patient’s hearing power. This, 
however, is a subject of such importance in otology that it seems better 
to consider it in a separate chapter. 

4 A clear and satisfactory statement of the technic of this procedure and the diffi¬ 
culties it may present will be found in Coakley’s “Manual of Diseases of the Nose 
and Throat.” 







CHAPTER III. 

FUNCTIONAL EXAMINATION OF THE COCHLEAR APPARATUS; 

HEARING TESTS. 

To the average practitioner of medicine the functional examination 
of the ears is an unknown art. If he has kept his medical knowledge 
intact as he received it from the medical school, he should be in a position 
to make a practical differentiation between the commoner nerve lesions. 
But if his patient suffers from impaired hearing, he can not by his own 
efforts determine whether this functional loss is due to an attack of acute 
tubal catarrh or to a lesion involving the labyrinth or auditory nerve. 
Nor is it an easy matter for him to gain from otological literature or text¬ 
books a practical working knowledge of the more important hearing tests, 
their rationale and the proper method of applying them. The author 
wishes, therefore, if possible, to present the essentials of this important 
subject in a form more easily available both by the busy physician and by 
the overworked medical student. 

Before we can draw any practical conclusions from a functional exam¬ 
ination, we must have in mind some normal standard of hearing with 
which to compare results. It will be remembered that the normal ear 
appreciates musical tones between two extremes of pitch,—the tone pro¬ 
duced by a sonorous body executing 18 double vibrations per second rep¬ 
resenting approximately the lower limit of normal hearing, and 41,000 
double vibrations per second representing the upper tone limit. 1 

Air Conduction and Bone Conduction of Sound. —Sound is brought 
to the organ of hearing in two ways,—(1) by air conduction, as when the 
vibrating body is at a variable distance from the ear, the sound waves 
being transmitted through the medium of the surrounding air; and (2) 
by bone conduction, as when the vibrating body is in contact with the skull, 
the sound waves being propagated through the solid medium of the cranial 
bones. Rinne demonstrated in 1855 that the human ear in health appre¬ 
ciates a given musical sound— e.g., that produced by the C tuning-fork 
(128 d. v.)—twice as long by air conduction as by bone conduction. This 
fact may be demonstrated in the following way: the fork having been 
thrown into maximum vibration, place the end of its handle in contact 

1 There can be no doubt that slight variations both as to the upper and lower tone 
limits may occur in different normal individuals. These variations possibly explain in 
part the different conclusions of different observers. Thus, Bezold, as a result of his 
examination of a large number of normal ears, placed the lower limit at 12 double 
vibrations per second. Helmholtz gave 32,500 double vibrations per second as the 
upper limit of possible tone perception. Politzer places it at 40,000 double vibrations, 
and Bezold at 41,000 double vibrations per second. 41,000 double vibrations correspond 
to the sound produced by the Edelmann-Galton whistle shortened to 0.5 and this may 
be accepted as the upper tone limit for the human ear. 


73 




74 FUNCTIONAL EXAMINATION: COCHLEAR APPARATUS 


with any portion of that side of the skull corresponding to the ear to be 
examined. The sound will be conveyed to the ear by means of the cranial 
bones. Request the person upon whom this test is made to indicate by 
raising his hand the exact moment, as nearly as he can determine it, at 
which the tone is lost to him. Now remove the fork from the skull and, 
without setting it in fresh vibration, bring the ends of the still vibrating 
prongs opposite the auditory canal of the ear to be examined. The tone 
will be again distinctly heard, and will continue to be appreciated during 
a period about equal to that during which it was heard through the cranial 
bones. In other words, it is heard by air conduction about twice as long as 
by bone conduction. This approximately l-to-2 ratio between bone conduc¬ 
tion and air conduction is one of the most constant functional characteristics 
of the normal ear, and is changed only in certain forms of aural disease. 

Normal Hearing Distances for the Watch=tick, the Acoumeter, the 
Conversational Voice and Whisper.—The experience of many observers 

in making a large number of hearing 
tests in persons with normal ears has 
established certain hearing distances 
for particular sounds as representing 
approximately the normal standard. 

The Watch-tick.- —This is a 
popular hearing test with the laity 
and medical profession alike. Natr 
urally this sound varies considerably 
in intensity with the size, form, thick¬ 
ness of covers, etc., of different 
watches. Taking, however, a man’s 
watch of average size, its tick will be 
heard by the normal ear of a young 
adult—say, of twenty to thirty-five 
years—at a distance of 40 to 50 
inches. This hearing distance is sub¬ 
ject to considerable variations within 
physiological limits, 30 inches not 
necessarily implying impaired hear¬ 
ing, and 60 inches falling within the hearing range of some individuals. 
As age advances, the hearing distance for the watch is gradually dimin¬ 
ished, and in old age— i.e., after sixty years—may be completely lost 
in individuals who, nevertheless, retain sufficient hearing power for 
the ordinary purposes of life. It is not always a reliable test of the 
usefulness of the organ, many persons whose hearing for the watch- 
tick is much below par having apparently no difficulty in interpreting the 
voice sounds in conversation. 

Politzer’s Acoumeter.— This very useful little instrument is so 
clearly shown by Fig. 74 that a detailed description is hardly necessary. 
The horizontal metal bar (a) is immovably attached to the upright column 
















THE CONVERSATIONAL VOICE AND WHISPER 75 

of hard rubber. The upper rod, or hammer, is movable so that when the 
short end (6) is depressed, the hammer is raised, and when the short lever 
is released, the hammer falls of its own weight, and, therefore, always 
with tne same force, upon the metal bar. It produces a clicking sound 
somewhat similar to the watch-tick, but ver}^ much louder. The different 
parts are of prescribed size and length, so that different instruments are 
supposed to produce approximately the same intensity of sound. The 
results of many tests have established 45 to 50 feet as about the normal 
hearing distance for the acoumeter. 

The Conversational Voice and Whisper.— This is the final test 
of the patient s hearing power as a means of communicating with the 
world of practical affairs. It is, therefore, the test in which he is most 
vitally interested. In making this test, the physician and patient stand at 
opposite ends of the room, the ear to be examined being turned toward 
the physician. The opposite ear is closed by a finger pressed firmly into 
the meatus. Standing thus sideways toward the physician, the patient 
can not see his lips, and the element of lip-reading is eliminated. The 
physician now repeats the words or numbers which he wishes to employ, 
the patient having been instructed to repeat them after him. If the patient 
can not hear, or hesitates or calls the words incorrectly, the physician at 
once moves nearer and repeats the experiment, using different words, 
but those having as nearly as possible the same sound values. The dis¬ 
tance between patient and physician is thus reduced until one is reached 
at which the words are repeated promptly and correctly. This is esti¬ 
mated in feet and carefully noted upon the test card. 

Owing to the difficulty in commanding always the same tone and 
intensity of voice, we are accustomed to test also with whispered words. 
In whispered speech, tone or pitch variations are practically eliminated, 
and it is much easier to cultivate a uniform intensity. Thus, one may 
employ a very low whisper, which can barely be heard by the normal ear 
at a few feet from the ear, or a very loud whisper, as when one partially 
fills one’s lungs and speaks the words without voice as forcibly as possible. 
Between the low and the forced whisper, a moderate whisper may be 
employed, which with a little practice may be made nearly, if not quite, of 
uniform intensity. Words spoken in the forced whisper can be heard by 
the normal ear at a greater distance than the same words spoken in a 
moderately low conversational voice, and the moderate whisper of one 
who has practised its use can probably be heard by the perfect organ of 
hearing at about the same distance as the moderately low speaking voice. 
Considerable time and effort have been expended by many distinguished 
students of otology in an attempt to determine the normal hearing dis¬ 
tance both for the conversational voice and for whispered speech. Owing 
to variations in pitch, timbre, volume, etc., in the voices of different 
individuals, and also to possible differences in clearness of enunciation, 
such questions can not be determined exactly. Making allowance for such 
voice variations, however, it may be said, probably with approximate 


76 FUNCTIONAL EXAMINATION: COCHLEAR APPARATUS 


accuracy, that the average conversational voice will be comprehended by 
the normal ear in a perfectly quiet room or hall at a distance of from 60 to 
70 feet, and that the whisper of moderate force will be heard at about the 
same distance. 

Recapitulation. —Defining briefly the functionally normal ear, we 
may say that an ear which hears the watch tick at a distance of 35 to 50 
inches, and the acoumeter 40 to 50 feet; which hears and correctly inter¬ 
prets the conversational voice and the whisper of moderate force at a dis¬ 
tance of 60 to 70 feet; which appreciates musical tones ranging between 
18 double vibrations and 41,000 double vibrations per second; and which 
hears a vibrating tuning-fork of 128 double vibrations, C, twice as long by 
air conduction as by bone conduction, is normal so far as its function 
is concerned. 

Before taking up in regular order the various tests by which we en¬ 
deavor to determine the site of an aural lesion, I wish to speak briefly of 
certain functional changes which occur quite regularly in advanced tym¬ 
panic disease, and of others which are equally characteristic of the deafness 
caused by labyrinthine or auditory nerve lesions. These functional 
changes are few in number; but once they are accepted as typifying the 
two main divisions of aural disease (t.e., tympanic and labyrinthine), it 
will be seen that the various functional tests are for the most part but 
convenient methods of establishing the presence or absence of changes the 
significance of which we already know. 

Changes in the Tone Limits.—Loss or Impairment of Hearing for 
the Lower Musical Tones. —It is a fact well known to otologists that 
lesions confined to the sound-conducting apparatus are almost invariably 
accompanied by some loss of hearing for the lower tones of the musical 
scale while the perception of high musical tones may be in no way inter¬ 
fered with. A very simple experiment will enable us to demonstrate this 
phenomenon as characteristic of tympanic disease. Ask a person with 
normal hearing to close both ears with a finger placed in each meatus. 
Now bring a vibrating tuning-fork of low pitch— e.g., of 26, 32, 36, 40, 43, 
or 48 double vibrations—in front of the auricle. Its sound will not be 
heard. Repeat this experiment with the C- 1 fork (64 d. v.) and its tone can 
not be excluded, while forks of still higher pitch— e.g., c 1 (256 d. v.)—are 
heard quite loudly in spite of any effort to close the external auditory 
canals. This loss of hearing for the lower musical tones occurs in stenosis 
of the Eustachian tubes, in chronic catarrhal otitis media, or as a result of 
occlusion of the external auditory meatus. In other words, lesions involv¬ 
ing any part of the sound-conducting mechanism interfere with the per¬ 
ception of low musical tones, the hearing for the high notes being affected 
comparatively little thereby. This phenomenon may seem a little more 
comprehensible if we bear in mind that very low musical tones represent 
long sound waves with slow vibrations of relatively great amplitude, 
whereas tones of high pitch are produced by short sound waves with rapid 
vibrations of very small amplitude. It is conceivable that mechanical 


INCREASED HEARING BY BONE CONDUCTION 


77 


obstacles to the movements of the ossicular chain would interfere first 
with the slower and greater excursions necessary to the transmission of the 
lower tones, and only in very advanced stages of ossicular fixation with 
the very rapid but slight excursions required to transmit the high musical 
tones. In elevation of the lower tone limit , or impaired audition for the 
lower musical tones, then, we have the first functional change which is 
characteristic of disease of the sound-conducting mechanism. 

Loss or Impairment of Hearing for the Higher Tones of the 
Musical Scale. —While not necessarily or invariably present, diminution 
or loss of hearing for the extreme upper tones of the musical scale occurs 
with sufficient regularity in diseases of the labyrinth or auditory nerve 
to justify a diagnosis of labyrinthine involvement in a majority of cases. 
This is rather difficult to understand, since it would at first seem that 
morbid processes within the labyrinth would be likely to involve any of 
the cochlear structures. It is known, however, that that portion of the 
basilar membrane which has to do with the perception of the higher musi¬ 
cal sounds is situated in the lower part of the cochlea,— i.e., in that part 
which is in most immediate relation to the foot-plate of the stapes and the 
membrane of the round window. It is believed that in most labyrinthine 
disorders (i.e., other than congenital deafness or deaf-mutism) this part 
of the cochlea and membrana basilaris is most frequently involved, and 
that the perception of the high tones is thereby interfered with. However 
this may be, it is a fact which clinical experience has abundantly confirmed, 
that with acquired lesions of the inner ear some loss of hearing for the 
upper end of the musical scale is almost invariably present. The author 
has repeatedly made functional tests in patients to whom half the notes of 
the Galton whistle were totally inaudible, whose lower limit was only 
moderately changed. Here, then, in lowering of the upper tone limit we have 
a counter functional change which points quite strongly to disease of the 
labyrinth, and we are prepared for our first step toward a differential 
diagnosis. 

Changes in the Period of Hearing by Bone Conduction. — In¬ 
crease. —To Schwabach is due the credit of having definitely established 
the fact—alread}^ partially demonstrated by Rinne—that in disease of 
the sound-conducting apparatus the period of hearing by bone conduc¬ 
tion is distinctly prolonged. This may be easily demonstrated by the 
following simple experiment: holding a vibrating tuning-fork in contact 
with the skull of a person of normal hearing, ask him to indicate by a 
motion of his hand the moment at which the tone is no longer perceived. 
Now, without removing the fork from the skull, require him to close both 
ears by a finger placed in each external auditory meatus. The sound cf 
the still vibrating fork will again be distinctly heard. In other words, we 
have created the mechanical equivalent of an obstructive lesion of the con¬ 
ducting apparatus with the result that bone conduction is increased. 

The explanation of the increase in hearing by bone conduction in 
tympanic disease proper is not altogether clear. Bezold believed that in 



78 FUNCTIONAL EXAMINATION: COCHLEAR APPARATUS 


bone conduction the sound is not transmitted directly through the cranial 
bones to the structures of the cochlea, but is conducted through bone to 
the drum membrane, or at least to the foot-plate of the stapes, and is 
transmitted thence to the labyrinth; in other words, that it is distinctly 
an osteo-tympanic conduction. In explanation of the increased bone con¬ 
duction regularly resulting from tympanic disease, he advanced the fol¬ 
lowing hypotheses: (1) That normally the whole conducting chain ■ 
drum membrane, ossicles, and annular ligament connecting the foot-plate 
of the stapes to the rim of the oval window—is in a state of perfectly 
mobile equilibrium. (2) That any abnormal or pathological condition 
within the tympanum, either b}^ changing the position of the stapes or 
inducing inflammatory changes in the region of the oval window, places 
the fibres of the ligamentum annulare in some degree on the stretch. (3) 
That stretching of the annular ligament interferes with the transmission of 
sound waves reaching the ear by air conduction, but distinctly favors the 
propagation of sound waves through the cranial bones to the foot-plate of 
the stapes. According to this theory it is also obvious that ankylosis of 
the stapes due to hyperplasia of connective tissue about the oval window 
should also tend to increase and prolong hearing by bone conduction. 

This theory, while not wholly convincing, is as satisfactory as any yet 
advanced so far as the writer knows. It does not, however, satisfactorily 
explain the increased hearing by bone conduction which occurs when the 
ear is closed by a finger placed lightly in the auditory meatus. This phe¬ 
nomenon, in the author’s opinion, is better explained as follows: In hear¬ 
ing by bone conduction part of the force of the vibrations thus transmitted 
is expended upon the column of air in the auditory meatus and thus con¬ 
veyed outward and dispersed through the medium of the surrounding 
atmosphere. When, however, a finger is inserted into the orifice of the 
meatus, this canal is converted into a closed cavity, and constitutes a 
resonance chamber in which the sonorous vibrations are collected and 
thrown back upon the drum membrane to augment those transmitted 
% directly from the cranial bones to the annular ligament and foot-plate of 
the stapes. That the increased perception of sound is brought about by 
the walls of this artificially closed cavity acting as resonators, and not by 
compression of the contained air, is shown by the fact that the sound is 
heard loudest when the finger tip is placed lightly in the meatus, and is 
reduced when the finger is forced deeply into the canal so as to produce 
condensation of the inclosed air. The phenomenon in its causation is 
somewhat analogous to the increased noise which we have all experienced 
in a railroad train during its passage through a tunnel. 

Leaving the question of its causation out of consideration, it is an 
established clinical fact that lesions of the conducting mechanism, not 
complicated by labyrinthine disease, are almost invariably accompanied 
by a prolonged period of hearing by bone conduction. The test for this 
phenomenon is as follows: Supposing the physician’s ears and hearing to 
be normal, he holds the handle of a vibrating tuning-fork in contact with 


DIMINISHED HEARING BY BONE CONDUCTION 


79 


his own mastoid process. As soon as he loses its sound the fork is trans¬ 
ferred, without renewing its vibration, to the mastoid of the patient. If 
he then perceives its tone, it may be assumed that his bone conduction is 
abnormally prolonged. Increased audition by bone conduction is the second 
and, in the author’s opinion, the most important functional sign of disease 
of the conducting apparatus. 

Diminished Hearing by Bone Conduction. —That the influence of 
labyrinthine or auditory nerve lesions upon hearing by bone conduction 
should differ from that exerted by tympanic disease hardly requires ex¬ 
planation. The labyrinth and auditory nerve with the cortical brain 
centres constitute the perceptive mechanism proper. When the hearing is 
impaired as a result of disease in any of these structures, it follows logically 
that the hearing power is diminished by all the normal pathways of sound 
transmission. Hearing is, therefore, reduced by bone conduction and air 
conduction alike. The test for this functional change is exactly the reverse 
of that by which we detect increase in bone conduction. The vibrating 
tuning-fork is first held in contact with the patient’s mastoid process cor¬ 
responding to the ear to be examined. When he indicates that its tone is 
no longer heard, the fork is transferred to the mastoid of the physician, 
—provided that his ears are functionally normal. If its tone is now dis¬ 
tinctly heard by him, the patient’s hearing by bone conduction is assumed 
to be less than normal. Loss or diminution of hearing by bone conduction 
is characteristic of all forms of labyrinthine or auditory nerve disease. 

We have, then, certain functional changes which show simply impair¬ 
ment of hearing, and which are met with in diseases affecting either the 
perceptive or the sound-conducting apparatus. Chief among these are 

(1) impaired audition for the watch or acoumeter, and (2) impaired hear¬ 
ing for the conversational voice and whisper. These changes do not 
materially aid us in locating the site of the lesion. 

Of differential changes— i.e., of functional changes characteristic of 
tympanic disease on the one hand, or of labyrinthine or nerve disease on 
the other—there are four which outrank all others in importance—viz.: 

Functional changes characteristic of disease of the conducting appa¬ 
ratus: (1) Elevation of the lower tone limit, or loss of hearing for the lower 
tones of the musical scale. (2) Increased, or prolonged, audition by bone 
conduction. 

Functional changes characteristic of labyrinthine disease: (1) Reduc¬ 
tion of the upper tone limit, or loss of hearing for the higher musical tones. 

(2) Diminution or loss of hearing by bone conduction. 

The writer believes that these changes in the tone limits and in the 
perception of sound as conveyed through the cranial bones, constitute 
the basic facts to be determined by our functional examination, and that 
the various differential tests are but convenient methods of demonstrating 
their presence or of determining their extent. 

There are many functional irregularities shown by different individ¬ 
uals suffering from chronic deafness,— e.g., disproportionate loss of hear- 


80 FUNCTIONAL EXAMINATION: COCHLEAR APPARATUS 


ing for certain sounds, as of the conversational voice as compared with 
the watch and acoumeter, or vice versa; disproportionate impairment for 
certain words or consonants, etc. In spite of much careful study of such 
changes by O. Wolf, Bezold, and others, they have not yet been sufficiently 
worked out to be of great practical value, either in locating the lesion or 
as an indication of the line of treatment to be pursued. We shall now 
take up briefly the method of applying the various tests. 

Method of Examination. — Watch and Acoumeter. In testing 
with a watch or acoumeter, the ear not under examination is closed by 
pressing a finger firmly into the orifice of the meatus. The watch is held 
for a moment close to the ear to be examined to familiarize it with the 
character of the sound. It is then removed four or five feet from the ear, 
and brought gradually nearer until its sound is heard, the distance in 
inches being noted. The experiment is now repeated once or twice for 
corroboration, the patient closing his eyes so that his imagination will not 
be stimulated by his knowledge of the position of the watch. The dis¬ 
tance thus finally reached is carefully noted upon the test card. 

It has been found that the watch-tick can be heard farther if the watch 
is first held close to the ear and the distance gradually increased than if 
the reverse method be employed,— i.e ., holding the watch outside of the 
hearing range and gradually approximating it to the ear. 2 The latter 
method is more reliable, since the imagination is brought less into play. 
If the watch sound can not be heard even when held within an inch of 
the ear, it should be placed in contact with the auricle, and the result, 
according to whether its sound can or can not be heard, should be thus 
noted upon the test card,—“heard only on contact,” or “not heard on 
contact.” In cases in which the watch is heard only on contact, or but a 
few inches from the ear, it is better to discard this test altogether and 
depend upon the acoumeter. One reason for this is the fact that such 
patients often make more or less pronounced functional gains for other 
sounds with relatively little change for the watch-tick; and again, the 
patient may so concentrate his attention upon his hearing for this particular 
sound as to become depressed or even neurasthenic because his functional 
gain as shown by this test does not seem sufficiently marked. With chronic 
aural disease as with other physical disorders it is desirable that the 
patient’s attention should not be focused upon his symptoms. In cases 
of slight impairment of hearing, however, the watch-tick affords a most 
useful test. 

The acoumeter is employed in exactly the same way as the watch except 
that one begins the test at a greater distance from the patient,—i.e., 
standing at the opposite end of the room. The result is noted upon the 
test card either in inches or feet, according to the degree of deafness. 

2 This phenomenon is explained by the fact that the individual’s power of auditory 
concentration and accommodation enables him to follow a sound once heard to a dis¬ 
tance greater than that at which it is first perceived when the sounding body is gradually 
moved toward the ear. 



SOUND VALUES OF DIFFERENT CONSONANTS 


81 


Whispered and Conversational Speech. —The patient’s hearing 
power for whispered and spoken words or numbers furnishes us with a 
quick and convenient method of determining functional impairment or 
loss. We can not employ this test intelligently, however, without some 
preliminary study of sound values ,— i.e., of the varying carrying power 
of the different letters, alone and in combination. 

Sound Values in Conversational Speech .—There are certain general 
facts which experience quickly impresses upon those coming in frequent 
contact with the partially deaf. We soon learn, for example, that the 
vowel sounds are heard farther and with greater distinctness than the 
consonants. A person with advanced catarrhal deafness may, therefore, 
hear the vowel sounds with comparative ease after the hearing for many of 
the consonants has become difficult, or possible only when they are spoken 
in loud tones. This fact explains the frequently repeated statement of 
the hard-of-hearing: “I hear your voice, but can not understand what 
you say.” It also explains the not uncommon experience, in testing the 
hearing of such a patient for spoken words, that he repeats not the word 
we have employed, but one having the same vowel sounds: thus, we call 
the word “faster,” and he says “master,” guessing at the initial consonant. 
Further than this, we find that certain consonants are heard better than 
others; that in testing with whispered numbers, those beginning with s— 
e.g., 67 or 76—may in some cases be heard easily at 20 or 30 feet, while 
numbers beginning with f or th— e.g., 53 or 35—are heard only with dif¬ 
ficulty at one-third of that distance. Or conditions may be reversed. 
Obviously the subject of sound values is one of considerable importance 
in practical otology. 

Of the vowels a, e, and i are heard farther than o and u. While it 
has long been known that the vowels each possess a distinct tone or pitch 
(Helmholtz), it remained for Oskar Wolf 3 to prove that the consonants 
also possess each its own tone. By this is meant that each consonant, 
spoken without voice (i.e., whispered) gives rise to a certain number of 
rhythmic vibrations per second, which determines its particular tone. 
This fact throws some light on the difficulties of the hard-of-hearing in 
interpreting conversational speech, for if the patients ear has lost the 
power of responding readily to the tone inherent in a certain consonant, 
he will hear this consonant poorly or not at all. It in such a case the con¬ 
sonant in question is spoken in a tone of voice falling within the patient s 
range of tone perception, he will hear the voice but will not distinguish 
the consonant sound. Hence his confusion in following the trend of 

conversation. 

The tones (pitch) inherent in the different letters are distributed rather 
widely over the musical scale. The letters 1, m, n, and r are in the lower 
half of the musical scale, while the self-tones of the sibilants, s and sh, 
belong to the upper half of the scale. Bezold found that deaf-mutes w ho 

3 Sprache und Ohr, akustisch-physiologische und pathologische Studien, 1871. 


6 







82 FUNCTIONAL EXAMINATION: COCHLEAR APPARATUS 


possessed “islands” of tone perception which included the self-tones of 
the principal consonants, could be taught by means of the ear to speak; 
but that deaf-mutes having “islands” of tone perception which did not 
include the self-tones of the consonants, could not be taught through the 
ear. 

The various elements of speech differ very considerably in the dis¬ 
tances at which they can be heard by the normal ear. The s and sh sounds, 
for example, carry farthest and can be heard three times as far as f, v, t, 
th, d, and k. Again, f, v, t, d, and k are heard farther than b or p. While 
it is not important that the aurist should know the exact hearing dis¬ 
tance for each consonant, it is quite essential that he should know and bear 
in mind that certain sounds are heard more easily than others. Thus, in 
the whisper test, the normal ear will be able to hear the words “sense” 
and “shine” farther than the words “pepper” and “five.” When, however, 
the hearing is impaired by disease, the relative auditory acuteness for 
different sounds may be changed. 

An approximate analysis of the relative loss of hearing for the different 
elements of speech may be made in the following way: Standing at a 
distance from the patient well beyond his range of hearing for the whisper, 
we begin our test with words or numbers spoken in a rather low whisper. 
It will be found that while most of the selected words are quite be3mnd his 
power of audition, certain words or numbers will be caught and repeated 
promptly and correctly. These words and the distance at which they are 
heard should be noted. We now move a few feet nearer the patient and 
repeat the test, when certain other sound values for this particular patient 
may be demonstrated, which also should be noted on the history card. 
The next step is to reduce the distance to a point where the patient can 
hear and repeat all words promptly and correctly. This distance must, of 
course, be recorded as representing his hearing distance for the moderately 
low whisper. We now possess rather definite data. Confining ourselves, 
for example, to the use of numbers, our results may read somewhat as 
follows: 

Right Ear: 

Moderately low whisper ,—6 feet (i.e., distance at which all numbers 
are heard). 

N-sounds, — e.g., 19, 9, 99,—9 feet. 

S-sounds ,— e.g., 16, 67, 76,—12 feet. 

Such functional reactions are by no means uncommon in chronic aural 
disease. With such a record, one would not be likely to fall into exag¬ 
gerated or erroneous conclusions as to a functional improvement when 
none had occurred. In other words, the haphazard use of words in test¬ 
ing is apt to lead to confusion, leaving the question of functional gain or 
loss in doubt. 

So distinguished an authority as the late Professor Bezold 4 advised 


4 Text-Book of Otology, p. 72. 






83 


DETERMINATION OF LOWER TONE LIMIT 

that we make use exclusively of numbers in our functional tests, express¬ 
ing his belief that we can obtain with numbers all the data that might be 
gained by testing also with words. My own actual experience has led me 
to a quite different conclusion in regard to this particular point. If in 
testing, either with conversational voice or whisper, we employ only num¬ 
bers, the patient quickly learns to associate certain sounds as the examiner 
utters them with the corresponding numbers, even though his actual hear¬ 
ing of them has not improved. His improvement is, therefore, more appar¬ 
ent than real. The writer believes that one should use words as well as 
numbers, the alternation ol the one with the other furnishing the very 
best criterion of the patient’s hearing power for conversational speech. 

The conversational voice is also a useful means of determining the degree 
of impairment, but is of little value as a test for purposes of comparison. 
In cases of very advanced deafness, however, even the forced whisper may 
be unavailable, in which case it becomes necessary to use the voice, speak¬ 
ing in a very loud and moderately high tone. In such cases one must 
depend upon other tests to demonstrate slight changes either in the way 
of functional gain or loss. 

Before leaving this subject, a word should be said as to the disparity 
between the estimated normal hearing distance for speech and whisper and 
the dimensions of the average testing room at the physician’s command. 
We must remember that the sole purpose of functional testing is to deter¬ 
mine the degree and character of the impairment. The aurist whose 
testing room is but 30 feet long soon learns to moderate the intensity of 
his whisper or voice in accordance with the space at his command, and his 
results are practically as reliable as they would be in a larger room or hall. 

Determination of the Lower Tone Limit (Figs. 75 and 76).—For 
this purpose a set of tuning-forks is essential. Hartmann’s set, consisting 
of five forks, supplies a convenient means of roughly estimating the lower 
tone limit in cases of very advanced catarrhal deafness. These forks 
represent C-tones one octave apart,— i.e., 128, 256, 512, 1024, and 2048 
double vibrations per second. But since the lowest fork of this series— 
i.e., 128 d. v.—is about three octaves higher than the lowest tone perceived 

tlie normal ear, a lower fork is required in cases of slight or moderate 
impairment of function. The large clamped fork (Fig. 76) is capable of 
executing either 26 or 64 double vibrations per second. With the clamps 
or weights attached to its prongs, it vibrates 26 times per second; and 
with the weights removed, 64 times per second. With this fork supple¬ 
menting the Hartmann set, we can determine positively whether the lower 
tone limit is appreciably elevated. While 26 d. v. does not represent accu¬ 
rately the lower limit of normal tone perception, this fork is the lowest 
employed in many aural clinics, it being assumed that if the patient clearly 
perceives its tone, his hearing for the lower musical notes can not be 
greatly reduced. 

In testing the patient’s hearing for the lower musical tones, he should 
be required to close the ear not under examination. Using first the low, 


84 FUNCTIONAL EXAMINATION: COCHLEAR APPARATUS 


clamped fork (26 d. v.), it is set in vigorous vibration and held near the 
external auditory meatus. If its tone is distinctly heard, it is assumed that 
his lower tone limit is normal, or nearly so; if heard but faintly and for a 
moment or two only, one may infer that the lower tone limit is elevated, 
and that the hearing for still lower tones— e.g., 18, 20, 21, and 24 d. v.—is 
lost. If not heard at all, the clamps should be removed from the fork, 


128 d.v. 256 d.v. 512 d.v. 1024 d.v. 2048 d.v. 



Fig. 75. —Hartmann’s tuning-forks. 


and the hearing tested for the next higher tone of this series of forks,— i.e., 
C- 1 , or 64 d.v. per second. If this also is inaudible to the patient, the hear¬ 
ing is tested with successively higher forks— e.g., 128, 256, 512 d. v., etc.— 
until one is reached which the patient can distinctly hear. This tone, or 
vibration rate, is then recorded upon the test card as the lower tone limit, 
— i.e., as nearly as it can be determined by this incomplete set of forks. 

In using so large and heavy a fork as that producing 26 vibrations per 
second, the patient may feel the vibrations yet not hear its tone, and this 








DETERMINATION OF LOWER TONE LIMIT 


85 


sensation he may mistake for tone per¬ 
ception. He must be made, therefore, 
to differentiate between the sensation 
due to the impact of the aerial move¬ 
ments upon the ear, and the per¬ 
ception of these movements as a 
continuous musical tone, or hum. If 
there be difficulty in making this 
difference clear to the patient, he may 
be required to describe the charac¬ 
ter of the sound, to state whether it 
is of high or low pitch, etc. If one ear 
only is involved, a comparison of the 
impression received by the opposite 
ear will usually remove any doubt as 
to whether the tone is heard by the 
diseased organ. Another possible 
source of error in the use of tuning- 
forks is the occurrence of overtones. 
In testing with unclamped forks,— e.g., 
that producing 64 d. v.,—one usually 
hears immediately after it is set in 
vibration not only its fundamental 
tone (C- 1 ), but also certain higher 
tones, or harmonics, and these may be 
the only sounds heard by the patient. 
This, of course, might lead the 
examiner to very erroneous conclu¬ 
sions. One may easily eliminate over¬ 
tones, however, by exerting moment¬ 
ary pressure with the thumb upon one 
of the prongs at a point as near as pos¬ 
sible to the handle or shaft. It is im¬ 
portant that this point be kept in mind. 

With the limited set of forks above 
described, it is obviously impossible to 
determine the lower tone limit exactly. 
They enable us, however, in the great 
majority of cases to arrive at correct 
conclusions as to the character of the 
lesion so far as we are able to deter¬ 
mine it from changes in the lower tone 
limit. For exact notation of the 
functional changes resulting from treat¬ 
ment, on the other hand, there is 
obvious advantage in the possession 




Fig. 76. —Large tuning-fork. 






86 FUNCTIONAL EXAMINATION: COCHLEAR APPARATUS 


of a set of forks by which the lower tone limit may be exactly deter¬ 
mined. For example, a patient may not be able to hear 128 d. v. 
(c), but may hear 256 d. v. (c'). Testing with the Hartmann set, we are 
obliged to note 256 cl. v. as the lowest tone heard by the patient. But 
there are six full tones between 128 d. v. and 256 d. v. The lower tone 
limit may, therefore, be 144, 160, 171,192,213, 240, or 256 double vibrations 
per second. If now, after treatment, the patient can hear 128 d. v., it 
makes a great deal of difference whether his lower tone limit previously 
had been 144 d. v. (d) or 256 d. v. (c')> for in the one case he would have 
gained a single note, and in the other his tone range would have been 
extended by an entire octave. 

Bezold’s Tuning-forks .—Undoubtedly the most complete set of instru¬ 
ments for detecting gaps in the range of musical tone perception is 
that of Bezold and Edelmann of Munich. This set consists of ten large 
forks provided with clamps by which the tone of each fork may be varied, 
four smaller unclamped forks, two organ-pipes, and a modified Galton 
whistle. These forks are heavy, somewhat cumbersome, rather expen¬ 
sive, and are not made in this country. They can be ordered, how¬ 
ever, through any reliable firm of instrument dealers, and enable one 
thoroughly to test the patient’s hearing throughout the entire range of 
normal tone perception. They were designed especially for detecting 
tone gaps or islands of hearing in partial deaf-mutes, for which purpose 
they are undoubtedly the most complete and perfect instruments made. 
For measuring the degree of functional impairment in the hard-of-hearing, 
on the other hand, the full set is certainly not required. 

For determining exactly the lower tone limit, the author in his private 
work makes use of a set of tuning-forks which were made for him accord¬ 
ing to his own specifications (Fig. 77). The prongs of these forks are of 
uniform width and thickness, the variations in pitch being regulated by 
gradations in their length. Without clamps they produce every full 
note from C- 2 (32 d. v.) to c 2 (512 d. v.), and by weighting forks C- 2 , D- 2 , 
and E- 2 notes corresponding to 16, 18, and 20 d.v. are obtained. These 
forks have proved most satisfactory and useful in the writer’s practice. 

Impaired hearing for the lower musical tones points to a tympanic 
lesion, and the loss of hearing for successively higher tones marks, as a 
rule, the progress of the disease. 

Determination of the Upper Tone Limit (Fig. 78).—Diminution, 
or lowering, of the upper tone limit is most easily determined by the Galton 
whistle. This is practically a closed organ-pipe provided with an ob¬ 
turator, by moving which the tube may be lengthened or shortened at will. 
As the tube, or pipe, is shortened, the length of the sound wave is short¬ 
ened and the vibration rate is increased. On the outer surface of the tube 
is a numbered scale,—0, 1, 2, 3, etc.,—provided with a mechanism by 
which changes in the length of the tube are indicated. By certain mathe¬ 
matical calculations these numbers and fractions thereof may be converted 
into the corresponding numbers of vibrations per second. This, however, 


87 


ALTERATIONS IN BONE CONDUCTION 

is not essential to piactical diagnosis, the numbers themselves soon be¬ 
coming associated in the aurist s mind with the normal in tone perception 
and certain degrees of departure therefrom. In testing with the Galton 
whistle, the instrument is held near the ear to be examined, the opposite 
ear being closed by a finger in the meatus. Air is propelled through the tube 
by compression of the rubber bulb attached to it. The patient will be likely 
to distinguish two sounds,— i.e., a puffing or blowing sound as of escaping 
ail, and a clear whistle. He should be required to indicate the point at 
which a clear whistle is heard. With the improved Bezold-Edelmann 
w histle, a clear note is heard with the marker at 0.5. Shortening the tube 
further than this, no clear whistle is heard. On the other hand, wdien the 
tube must be lengthened beyond 0.5 in order to obtain a note audible to the 
patient, it becomes ev ident that his upper range of tone perception is 
lowered. Some diminution of hearing for the extreme upper tones of the 
musical scale is physiological in old age, and may occur in certain disorders 
of the general nervous system. Generally speaking, however, any appre¬ 
ciable diminution of hearing for the upper musical tones in a person not over 
fifty years of age points either to a labyrinthine or nerve lesion, or to some 
aural disorder in which the labyrinth is secondarily involved. 

An ingenious mechanism, which, if it could be made generally available, 
would add greatly to the accuracy and scientific value of our hearing tests, 
is the so-called tone-range audiometer devised by Dr. Lee Wallace Dean 
and Mr. C. C. Bunch, of the State University of Iowa. 5 Roughly speaking, 
this instrument consists of an electrically driven toothed wheel, the cogs of 
which come successively in contact with a magnet, the tone being produced 
by the rhythmic opening and breaking of the circuit. It is said to produce 
an approximately pure musical tone, the intensity of which can be controlled, 
and the pitch of which can be rapidly or slowly elevated or lowered between 
the tonal limits of 30 and 10,000 double vibrations. The advantages of such 
an instrument over tuning forks in the detection of gaps in tone perception 
are obvious. As with every notable advance in diagnostic method and 
accuracy, it is probable that this mechanism in the hands of its distinguished 
inventor will add to our scientific knowledge of disease by establishing shades 
of functional difference between certain closely related lesions,—shades of 
difference not definitely determinable by the older methods. 

Changes in Hearing by Bone Conduction. —There are two methods 
of determining changes in the duration of hearing by bone conduction, one 
of which has already been mentioned. Assuming the examiner’s ears to be 
functionally normal, the handle of a vibrating tuning-fork of 128 d.v. (c) 
is held in contact with his own mastoid process, and transferred as soon as 
its tone is no longer heard to that of the patient corresponding to the ear to 
be examined. If its tone is distinctly heard by him, it is inferred that bone 
conduction is increased; and if we count the number of seconds during which 
it is heard by the patient and find this to be, say, 10 seconds, we may record 


5 Dean and Bunch: Audiometer: Laryngoscope, August, 1919. 




88 FUNCTIONAL EXAMINATION: COCHLEAR APPARATUS 


this result upon our test card as follows: “B. C., fork 128 d. v., increased 
(+10 seconds). ” If the sound of the vibrating fork thus transferred from 
the physician’s to the patient’s mastoid is not heard by the latter, we may 
assume at least that bone conduction is not increased. The reverse experi¬ 
ment is now tried,— i.e., the vibrating fork is held first against the patient’s 
mastoid and transferred, when its tone becomes inaudible, to that of the 
examiner. If its tone is now audible to the physician, we know that the 
patient’s hearing by bone conduction is diminished; and the degree of dimi¬ 
nution will be determined by the length of time during which it is heard by 
the physician. Supposing this to be 10 seconds, the result may be noted 
thus: “B. C., fork 128 d. v., diminished (-10 seconds).” If the patient’s 
duration of hearing is neither more nor less than that of the examiner, his 
bone conduction is charted “normal.” 

The method of examination just described is convenient and quite re¬ 
liable so long as the examiner’s ears, and particularly his hearing by bone 
conduction, conform to the normal standard. So soon, however, as his 
hearing becomes impaired, it is obvious that he will no longer be able to 
make correct deductions from a comparison of the patient’s hearing with 
his own. If we wish to reduce this test to an absolutely correct basis, it is 
necessary that we should know the normal duration of hearing by bone con¬ 
duction for certain forks, and determine whether the patient’s hearing con¬ 
forms to this standard. The corresponding forks of different sets vary, 
however, in the intensity of sound produced and in the period during which 
they can be heard. It is necessary, therefore, that the aurist should deter¬ 
mine for himself the normal sound duration for his particular forks to be 
used in this test. This can be done with approximate accuracy by testing 
them {i.e., determining in seconds their sound duration) upon a certain num¬ 
ber of supposedly normal ears, which also show a normal standard as 
gauged by other tests,— e.g., watch, acoumeter, whisper, Rinne, etc. And as 
two forks— i.e., the 128 d. v. and 256 d. v. forks of the Hartmann set—will 
suffice for all tests of bone conduction, it is not a difficult matter to determine 
their normal period of sound transmission through the cranial bones. In 
testing by this method, the fork should be struck forcibly, to obtain its maxi¬ 
mum vibration, and the handle at once placed in contact with the mastoid 
process of the ear under examination. The number of seconds during which 
its sound is heard by the patient should be counted by means of a stop watch. 
Supposing, for example, that we are using a fork the normal duration of 
which has been found to be 20 seconds, it is an easy matter to determine 
by how many seconds the patient’s hearing by bone conduction is either in¬ 
creased or (diminished. This method of testing bone conduction is given as 
the only one open to the physician who is himself the victim of advanced 
aural disease. With fairly normal ears, however, the first method is much 
quicker, infinitely more convenient, and yields sufficiently accurate results. 

Impairment or absolute loss of hearing by bone conduction in one ear is 
sometimes difficult to determine, from the fact that the sound may be trans¬ 
mitted through the cranial bones to the opposite ear. Usually, however, 


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00 


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a 


c > 

W 9 



ei ^ 

I "3 
O CO 


CJ 

I 

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CO 

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o 


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. . ■■■■.■..■■■■■■ • •■ ■ •■•■■ . • ■ ' 



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Fig. 77. —Kerrison’s set of tuning-forks. 


The number opposite each fork corresponds to the number of double vibrations which that par¬ 
ticular fork (in producing its fundamental tone) executes. The number opposite forks C-*. D-, and 
E- 2 indicate the number of double vibrations which these forks execute when the clamps are removed. 
With the clamps adjusted and moved to different positions upon the prongs, much lower tones—i.e., 
tones corresponding to 14, 16, 18, 20, 22, 24, and 26 double vibrations per second—can be produced 



Fig. 78.—Galton whistle, 


106. 66 d.v. 12S d.v. 144 d.v. lOOd.v. 192 d.v. 240 d.v. 288 d.v. 341. 32 d.v. 4 20. 66 d.v. 512 d.v. 

H-i f a c l ei g 1 hi 

120 d.v. 170.66 d.v. 213. 33 d.v. 256 d.v. 320 d.v. 384 d.v. 480 d.v. 



























































































































































SCHWABACH’S TEST: RINNE’S TEST 


89 


one can obtain sufficiently positive data to enable one to draw correct con¬ 
clusions as to the character of the lesion. 

Having tested the patient’s hearing both as to the tone limits and as to 
changes in bone conduction, we are in a position to form a fairly definite 
opinion as to the site of the lesion. In the writer’s opinion, further tests, 
while of undoubted value, are for the most part corroborative. That is to 
say, with elevation of the lower tone limit and increased bone conduction, 
the hearing for rhe upper tones remaining normal, the inference is definitely 
in favor of disease confined to the conducting apparatus. If, on the other 
hand, the upper tone limit is lowered, the lower limit but little changed, 
and hearing by bone conduction is decidedly diminished, we are not likely to 
prove in error in concluding that the labyrinth or nerve is chiefly at fault. 

Schwabach’s Test .—Schwabach attempted to determine the periods in 
seconds during which tuning-forks of different pitch are heard through the 
cranial bones by the normal ear. He proved that there is an absolute in¬ 
crease in bone conduction in diseases of the conducting apparatus. His 
test, therefore, proposed the determination of the patient’s duration of hear¬ 
ing by bone conduction of a large number of forks, and their comparison 
with the normal standards therefor. This test adds little to the knowledge 
obtained from the simpler experiment by which increase or diminution of 
bone conduction is determined. Its results are corroborative. 

Rinne’s Test. —Rhine’s experiments proved two things,—viz.: (1) that 
the normal ear hears a vibrating tuning-fork twice as long by air conduction 
as through the cranial bones, and (2) that in tympanic disease this ratio be¬ 
tween air conduction and bone conduction may be absolutely reversed. The 
c fork (128 d. v.) and the c' fork (256 d. v.) of the Hartmann set are appro¬ 
priate for this test. For young adults the c' fork is preferable, but with pa¬ 
tients past middle life, in whom hearing by bone conduction is physiologically 
reduced, the c fork (128 d. v.) gives more reliable data. Rinne’s test is ap¬ 
plied in the following way: the fork is set in vigorous (maximum) vibration 
and the handle at once placed in contact with the mastoid corresponding to 
the ear to be examined. As soon as the patient indicated that its tone is no 
longer heard, the fork is removed from contact with the cranium and the 
ends of the still vibrating prongs are brought near to and opposite the orifice 
of the meatus. If now he again hears its tone and continues to hear it during 
a period approximately equal to its duration by bone conduction, we must 
regard this as the normal ratio between hearing by bone conduction and by 
air conduction. This in otological literature is spoken of as a “positive 
Rinne It may be found, however, that after hearing by b. c. ceases, the 
patient will no longer be able to hear by a. c. I his, of course, points to dis¬ 
ease, or at least derangement, of the conducting apparatus. We must now 
• reverse the experiment, holding the vibrating fork first in fiont of the ear, 
and transferring it when its sound is no longer heard to contact with the mas¬ 
toid. It is possible that its tone will again be heard through the cranial 
bones during a period about equal to its previous duration by aii conduc tion. 
This reversed ratio indicates advanced tympanic oisease, and is spoken of 


90 FUNCTIONAL EXAMINATION: COCHLEAR APPARATUS 


as a “negative Rinne.” This is one of the most reliable and useful tests of 
chronic middle-ear disease. No other functional test shows so graphically 
the various stages of functional impairment. Thus, in the earliest stages 
of tympanic disease the hearing by a. c. will be very slightly diminished 
while the hearing by b. c. will be very slightly increased. The ratio be¬ 
tween b. c. and a. c. will, therefore, not be reversed, the peiiod of hearing 
by a. c. after hearing by b. c. has ceased being simply shortened. This 
is spoken of as a “diminished positive Rinne. ” 

The diagnostic significance of the various reactions to this test in uni¬ 
lateral aural disease may be stated as follows: 

A. Hearing noticeably impaired, Rinne negative, the ratio between b. c. 
and a. c. being reversed; these reactions would point to an advancd lesion 
of the conducting apparatus. 

B. Hearingnoticeably impaired, Rinne positive, t he ratio between b .c. and 
a. c. being normal, would suggest disease of the labyrinth or auditoiy nerve. 

C. Hearing not appreciably impaired, Rinne positive and showing 
normal ratio, would suggest a normal ear. 

D. With hearing but slightly impaired, a “diminished positive Rinne” 
would indicate a comparatively early stage of tympanic disease. In such 
a case the progress of the lesion is likely to be marked by progressive short¬ 
ening of the period during which hearing by a. c. outlasts hearing by b. c. 

The prognostic value of this test is indicated by the following fact, as to 
the correctness of which I am sure that all experienced aurists will bear me 
out,—viz., that when, as a result of chronic or slowly developing tympanic 
disease, the ratio between b. c. and a. c. is absolutely reversed, the hearing 
may be improved by treatment, but can never be restored to the normal 
standard. 

Weber’s Test .—This consists in holding the handle of a vibrating tuning- 
fork (128 d. v. or 256 d. v.) in contact with the median anteroposterior line 
of the vertex of the skull. The sound will be transmitted through the cranial 
bones, and, since bone conduction is increased in tympanic disease, the 
sound will be conducted in greater volume to the diseased ear in all uni¬ 
lateral lesions of the conducting mechanism. The patient, therefore, has 
the impression of hearing it altogether with the diseased ear. On the other 
hand, if hearing by bone conduction is diminished in the diseased ear, as is 
the case in lesions of the labyrinth or auditory nerve, the sound will be appre¬ 
ciated chiefly by the normal ear. In unilateral deafness, therefore, the 
sound of a tuning-fork held in the mid-line of the skull will be referred by the 
patient to the diseased ear if the lesion is located in any part of the conduct¬ 
ing apparatus, and to the sound ear if the disease is confined to the labyrinth 
or auditory nerve. It is a recognized fact that in certain individuals with 
perfectly normal ears the hearing by bone conduction may be referred 
chiefly to one side or the other, purely as a result of inequalities in the thick¬ 
ness, or other anatomical differences, between the opposite sides of the skull. 
This, however, is exceptional. In the average run of cases Weber’s test is an 
easily applied and useful corroborative test, confirming what we have 


TOTAL DEAFNESS 


91 


already learned as to the relative increase or diminution of bone conduction 
in one ear as compared with the other. 

Gelle s Test. This test is dependent upon the fact that any force exert¬ 
ing sudden inward pressure upon the stapes pushes this ossicle farther into 
the oval window and, by increasing intralabyrinthine pressure, reduces 
tone perception, whether the sound wave has reached the tympanum by 
air conduction or by bone conduction. Gelle’s experiment consists of con¬ 
densing the air in the external auditory meatus by means of a Siegel’s 
speculum and bulb, or similar apparatus, a vibrating tuning-fork being 
held, meanwhile, in contact with the skull. Normally, as the drum men- 
brane and ossicles are forced inward, intralabyrinthine pressure is increased 
and the sound of the tuning-fork is thereby diminished. As the pressure 
upon the drum membrane is removed, the stapes n oves outward, intrala¬ 
byrinthine pressure regains its equilibrium, and the sound of the vibrating 
fork increases in volume. In this way the intensity of the sound may be alter¬ 
nately increased and diminished. It is held that when tympanic changes 
causing fixation of tne ossicles have occurred, the labyrinth will not be 
affected by condensation of air in the external auditory meatus, and hearing 
by bone conduction will not be diminished. A negative result is, therefore, 
held to point to ossicular fixation. So far as the writer can see, this test is of 
theoretic value in only one condition,—viz., when the stapes is firmly fixated 
or immobilized, within the oval window. It is not of great practical value 
in diagnosis. 

Bing's Test .—This experiment is mentioned in most text-books as a 
means of differentiating labyrinthine from tympanic lesions. A vibrating 
tuning-fork is held in contact with the skull,—preferably upon the mastoid 
process of the ear to be tested. As soon as its tone can no longer be heard, 
a finger is introduced into the external auditory meatus. It is claimed that 
the tone will again be distinctly heard if the disease be located within the 
labyrinth, but will not be heard, or will be heard but faintly and during a 
diminished period, if the lesion be confined to the tympanum. This test 
is somewhat unreliable from the fact that in the early stages of either 
labyrinthine or tympanic disease the sound will recur after closure of the 
meatus, and in very advanced stages the experiment is likely to give nega¬ 
tive results whether the disease be located within the labyrinth or the 
middle ear. With marked increase in bone conduction, one is not likely to 
think of labyrinthine disease because the sound of a vibrating fork held 
against the skull can be prolonged by closing the meatus, nor will one doubt 
labyrinthine disorder in the presence of marked diminution of bone con¬ 
duction because this experiment results negatively. 

Total Deafness. —In the foregoing pages we have described the 
various hearing tests which are of use in the analysis of partial deafness,— 
i.e., the impairment of such patients as are commonly spoken of as “hard 
of hearing.” Practically all cases of functional impairment due to tym¬ 
panic disease, and many cases in which the perceptive mechanism is also 
involved, come under this classification. There is, however, another class 


92 FUNCTIONAL EXAMINATION: COCHLEAR APPARATUS 


of cases in which many of these tests are of little or no value,—I refer to 
cases of bilateral or unilateral impairment so great as to approach or actu¬ 
ally to constitute total deafness. When one ear is very nearly or totally 
deaf and the other ear retains in large degree its quota of hearing power, 
the possibilities of error in diagnosis are not inconsiderable. Cases have 
come under the writer’s observation in which the patient has been sub¬ 
jected to much useless treatment simply because a careless or inexperienced 
practitioner had failed to recognize the fact that one or the other ear was 
totally or hopelessly deaf. Such profound deafness always means disease 
of the cochlea or of the auditory nerve. A word must therefore be said 
as to the determination of profound or total deafness. 

Total bilateral deafness is not difficult to determine. In the first case, 
the patient is unable to hear a word that is said, even though it be spoken 
in a loud voice or shouted close to the ear. With tuning-forks also, unless 
there be remaining islands of tone perception, he hears no sound. It 
sometimes occurs with tuning-fork tests that the patient receives the 
impression that he hears the sound when in reality he only feels the impact 
of the aerial vibrations against the skull. This is particularly apt to occur 
when we use a large fork in maximum vibration. We are usually able to 
detect this error by his inability to describe the sound correctly. 

With total deafness, bone conduction also is lost. But here again we 
must guard against apparent contradiction resulting from the patient’s 
inability to differentiate between his sense of the vibrations against the 
skull and tone perception. 

Absolute Deafness in One Ear. —This, when the opposite ear is function¬ 
ally normal or nearly so, may be difficult to determine. The tuning-fork 
tests of tone perception, for example, present the following difficulties. 
With the normal ear closed by a finger in the meatus, the patient can not 
hear the lower musical tones,— i.e., tones from 18 to 42 d. v. But when 
we reach 64 d. v., or a little higher, it will be found impossible to exclude 
its tone from the normal ear, however tightly it be closed. If now he be 
directed to close both ears, and still can hear the tuning-fork and with 
equal intensity, we may conclude that it is heard only by the sound ear. 

Loss of hearing by bone conduction may be even more difficult to deter¬ 
mine from the fact that tones of a vibrating tuning-fork held at any point 
on the skull may be transmitted through the cranial bones to the sound ear. 
It is best to begin by holding the fork in contact with the mid-line of the 
skull (Weber). The patient usually states that the sound is heard alto¬ 
gether by the normal ear. The experiment is now several times repeated, 
selecting each time a point nearer the diseased ear. If finally, with the 
tuning-fork in contact with the mastoid of the diseased ear, the patient 
still refers its sound to the healthy organ, we may be sure that hearing by 
bone conduction is completely lost in the ear under examination. Un¬ 
fortunately, the value of this test may be negatived by the patient’s 
inability to interpret correctly his own impressions. 

With many of these cases the final test of profound or total deafness is 


MALINGERING; SIMULATED DEAFNESS 


93 


the patient’s inability to hear the conversational voice. Voice sounds may, 
however, be heard by the sound organ, even though it be closed by a finger 
tightly pressed into the meatus. To meet this difficulty we have a reliable 
instrument in Barany’s noise apparatus (Fig. 79). This consists essentially 
of a small metal box provided with an ear-piece and containing clock-like 
machinery which when wound up produces a continuous rough metallic 
sound. It is used as follows: The ear-piece is introduced into the canal 
of the sound ear and by pressure upon a button the machinery is set in 
motion. While this sound is being poured into the normal ear, words 
or numbers are spoken in a loud voice close to the diseased ear. If they are 
not heard, we may be sure that the ear under examination is totally deaf. 
If the words are heard, we may be equally confident that they are not 
heard by the ear into which the noise apparatus is pouring its sound, and 
that the diseased ear is, therefore, not totally deaf. 

While the profound type of deafness above described is never met with 
in lesions confined to the conduct¬ 
ing apparatus, it is the rule in 
certain lesions of the inner ear,— 
e.g., diffuse suppurative labyrin¬ 
thitis. In such cases Barany’s 
noise apparatus, or some similar 
instrument, is absolutely essential. 

Malingering; Simulated Deaf¬ 
ness .—Pretended deafness is said to 
be comparatively common in coun¬ 
tries where army service is com¬ 
pulsory. In America it is met with 
chiefly in the case of impostors seek¬ 
ing indemnity on account of pre¬ 
tended injuries to one or both ears. 

Simulated bilateral deafness, if the individual persistently refuses to 
give evidence of any hearing power, is naturally difficult to detect. To 
disprove complete bilateral deafness, one must depend on one’s ability to 
catch the individual off his guard. It has been suggested that by making 
disparaging remarks about him in the presence ol a third part} 7- one may 
be able to determine by changes in his facial expression his ability to hear 
the conversational voice. Usually, however, the pretense of complete 
bilateral deafness is too difficult to maintain, and as a rule it is unilateral 
deafness the genuineness of which the aurist is called upon to determine. 

There is no absolutely reliable test for feigned deafness, the astuteness 
of the malingerer and the cleverness and knowledge of the physician being 
elements at play in every case. The following are among the tests employed. 

1. Assuming in a given case the lesion to be confined, to the sound-conducting 
mechanism, a vibrating tuning-fork is held to the mid-line of the skull (Webei). Its 
sound should be referred to the side of the lesion; the malingerer naturally states that 
it is heard by the sound ear. 

2. Testing the patient’s hearing for whispered speech through a tube dividing 



Fig. 79.—Barany’s noise apparatus. 



94 FUNCTIONAL EXAMINATION: COCHLEAR APPARATUS 


terminally into two smaller tubes—one for each ear—he is asked in which ear the words 
are heard. If the terminal tube communicating with the sound ear be blocked or closed, 
and he claims that the words are heard only by the presumably sound ear, it is assumed 
that the deafness in the opposite organ is not real. 

3. When only partial deafness is claimed, the various tests— e.g., as to hearing 
distances, tone limits, etc.—are made. Repeating these tests, the malingerer’s memory 
usually fails him, and his conflicting statements are likely to show that his answers 
are not to be relied upon. 

4. The individual having been blindfolded, the examiner stands behind him, and 
alternately tests the two ears rapidly with various forks. This frequently confuses the 
malingerer and brings answers so conflicting and contradictory as to demonstrate his 
lack of good faith. 

5. A device which the writer recently hit upon was conclusive so far as the case in 
question was concerned. The patient had received an injury in the course of his work 
for a large commercial company, and claimed to have become deaf in his right ear. 
For this he proposed to sue the company. The drum membrane appeared normal. 
His answers to the usual tests showed a degree of deafness which could only have re¬ 
sulted from a labyrinth injury. Arguing that such a disturbance of the cochlea would 
be likely to involve also the vestibular mechanism, the writer made a caloric test of the 
presumably deaf ear. This resulted in a quick and normal reaction, and during the 
confusion incident to the induced vertigo, it was easy to determine that his apparent 
unilateral deafness had been assiuned. 

Since the above was written, American aurists have acquired much prac¬ 
tical knowledge in the application of these tests in the examination of men 
striving to evade military service on account of pretended deafness. It 
may, therefore, be worth while to state briefly the tests which the writer, as 
a member of an advisory examining board, found most useful, and to describe 
the routine method of applying them. 6 

In the first place, let me emphasize the fact that it is important in dealing 
with a suspected malingerer that he shall receive no slightest hint that he is 
under suspicion. The more unsuspecting and credulous the examiner may 
appear, the more readily and conclusively will the suspect respond to the 
tests. The most glaring evidences of deception should therefore pass without 
comment or apparent notice until the examination is completed. 

Most malingerers of deafness who are subject to the military draft know 
that deafness of a certain grade in either ear will exempt them from service. 
Complete bilateral deafness is, therefore, for various and obvious reasons 
rarely, if ever, claimed. 

Two types of unilateral deafness are assumed, i.e., (1) deafness advanced 
but not complete; and (2) absolute deafness. 

My own routine method of examining these cases is about as follows: 
Only one man at a time is admitted to the examining room. I learn from 
him which is the deaf or deafer ear, and whether he regards this deafness 
as partial or complete. If only one ear is complained of, I make a rapid test 
of the better ear to determine that it is functionally sound or at least only 
slightly subnormal. This preliminary testing of the sound ear is essential to 
a proper interpretation of the tests to be applied later. 

Weber’s Test .—I now apply a vibrating tuning fork of 256 double vi¬ 
brations to the vertex of his skull, and if he refers the sound to his supposedly 

6 The following pages are taken almost verbatim from a report by the writer made 
before the American Otological Society in June, 1918. 



LOMBARD’S TEST 


95 


deaf ear, I am favorably impressed as to his honesty. If he refers it to his 
sound ear, I become skeptical, and proceed to the next test. 

Loud Voice Test .—The suspect’s eyes are now blind-folded. Requesting 
him to close with a finger his better ear, which has already been determined 
to be approximately sound functionally, I repeat words and numbers to 
him at first in a low voice and then in progressively higher and louder tones. 
If, when I have reached a pitch and intensity at which he should be able to 
hear and interpret the words with his sound ear even though tightly oc¬ 
cluded, he still states that he cannot hear them, I know at least that he is an 
intentional malingerer. This is a useful test which will expose many 
impostors. An alert individual, however, may throw this procedure out 
of court by stating that he hears the sound through his occluded normal ear. 

Stethoscope Test .—For this the ordinary clinical stethoscope with funnel- 
shaped chest piece is used. One ear piece is completely occluded with wax. 
Occlusion with cotton will not exclude the sound. Standing behind the 
examined, the stethoscope is adjusted with the occluded ear piece in his 
“deaf ” ear. Words in a low voice are spoken into the funnel-shaped chest 
piece, which naturally he should hear perfectly. The stethoscope is 
removed for the ostensible purpose of trying some other test, and then re¬ 
placed, the occluded ear piece being this time placed in his sound ear. If 
he is able to hear now approximately as well as before, we have fairly sound 
evidence that his deafness is either assumed or grossly exaggerated. This is 
a fairly reliable test. 

Tests for Eliciting Contradictory Responses .—The eyes are now uncover¬ 
ed, the sound or better ear is closed with a finger, and the “deaf” ear is 
rapidly subjected to the commoner classical tests, e.g., hearing distance for 
watch, acoumeter, whisper or conversation voice; tuning fork tests to de¬ 
termine lower tone limit, etc. His responses, so far as he admits hearing in 
any of these tests, are carefully noted. Following this, he is again blind¬ 
folded and the same tests are repeated many times, fairly rapidly and in 
varying order. If he is a malingerer and has not in the first instance claimed 
almost total deafness, his responses will almost surely demonstrate incon¬ 
gruous and contradictory variations. 

Lombard's Test .—This test, which requires a Barany noise apparatus, 
is one of the most dependable means of determining absolute or very ad¬ 
vanced deafness confined to one ear. It depends upon the fact that to the 
normal man the sound of his own voice is necessary to the regulation of its 
tone and intensity. It is carried out as follows: the noise apparatus is 
adjusted to his sound ear and its machinery started in order to accustom 
him to its grating noise. He is given a book and told to read aloud in his nat¬ 
ural voice and not to stop reading when the noise instrument is set in 
action. As soon as the noise begins, a man whose opposite, or open, ear is 
profoundly deaf will it once raise his voice, and if his deafness is absolute he 
may literally shout. The malingerer, on the other hand, claiming a one¬ 
sided deafness which is not real, will continue to read in an even tone or in a 
tone only slightly elevated. This is a test which a malingerer who has been 


96 FUNCTIONAL EXAMINATION: COCHLEAR APPARATUS 


coached may easily turn to his advantage. Otherwise it is one of the most 
useful at our disposal. 

Cochleo-palpebral Test (Gault ).—This test depends on the fact that if a 
sudden and unexpected noise is produced near either ear, there occurs a 
slight winking movement, or contraction of . the lids, in the corresponding 
eye. If, therefore, in a case of supposedly unilateral deafness, the sound ear 
is tightly closed and a slight noise, produced near the ear under suspicion, is 
followed by a contraction of the lids, however slight, on the same side, this 
is accepted as evidence of the sound having been heard in the ear in which 
deafness is claimed. It is clear that this test might be even more valuable 
in the case of a clever malingerer claiming bilateral deafness, when a notice¬ 
able palpebral contraction in response to a slight noise might constitute the 
only proof of the unreality of the auditory defect. 

Bilateral Deafness.—Naturally, as there are many cases representing all 
grades of bilateral deafness, malingering may take the form merely of an 
exaggeration of an existing defect. If such a person were persistently to 
assume absolute or very profound bilateral deafness, it is difficult to say what 
tests would expose the deception. The time-honored tricks of attempt¬ 
ing to ensnare him by a sudden and startling question, the use of insulting 
or disparaging remarks, etc., may be of value in certain cases but are cer¬ 
tainly not to be relied upon. The majority of malingerers, however, do not 
pretend to complete deafness. This is a fortunate fact for the reason that 
partial though disabling deafness burdens the malingerer with the necessity 
of maintaining uniformity in his responses to the various tests. The surest 
means of exposure in such cases is the application of the various classical 
tests first to one ear and then to the other, and then, after blind-folding him, 
repeating the same tests and comparing the two sets of responses. In my 
opinion, the most useful single test is the repeated determination, using a 
full set of tuning forks, of what he claims to be the lower limit of tone per¬ 
ception in each ear. In such repeated tests, a man would have to possess 
both a phenomenal memory and a wonderfully trained musical ear to avoid 
conflicting replies. 


CHAPTER IV. 

DISEASES OF THE EXTERNAL EAR (AURICLE; EXTERNAL 

AUDITORY MEATUS). 

INFLAMMATORY DISEASES OF THE AURICLE. 

Traumatic Auricular Dermatitis. —This condition is occasionally seen 
as a result of the slighter injuries to the ear,— i.e., injuries resulting in 
contusion or abrasion of the cuticle, but not seriously involving the 
perichondrium. It begins as a simple erythema, is usually accompanied 
by some degree of pain and sensitiveness to touch or pressure, and soon 
spreads more or less widely over the auricle. To establish its traumatic 
origin, it must be traceable to an abrasion or injury of the skin at the ori¬ 
fice of the meatus or at some point on the pinna. It may run its course as 
a simple erythema or, developing localized points of infection, become 
pustular in character. Such a lesion, unless too long neglected, is usually 
quite responsive to treatment. 

The treatment should begin with thorough cleansing of the part. 
If for this purpose an antiseptic drug is required, a solution of carbolic 
acid, 1 to 200 parts, is preferable to bichloride of mercury, which in itself 
is too irritating to the skin. After cleansing, the auricle should be thor¬ 
oughly dried, and an antiphlogistic ointment or lotion applied, according 
to the severity of the inflammation. If of very acute type,— i.e., of suf¬ 
ficient severity to cause considerable pain or discomfort,—it is well at the 
beginning of treatment to protect the ear by means of a large dressing of 
sterile gauze. The ointment or lotion may be applied upon a thin layer of 
gauze, and a dry gauze dressing applied over this. It may be said, however, 
that in many cases dermatitis of this type will make a perfectly satis¬ 
factory recovery without other treatment than cleansing of the part and 
protection from fresh injury. 

Erysipelas of the Auricle. —This disease may be secondary to the 
traumatic lesion above described, or it may have its origin in some slight 
injury or abrasion of the auricle or auditory meatus. Erysipelas of the 
auricle does not differ materially from the same lesion in other parts of the 
body. It rarely remains localized in the auricle, usually spreading to some 
extent to the face and scalp, so that it is apt later to assume the character¬ 
istic features of facial erysipelas. The redness, swelling, and tenseness of 
the skin are much more marked than in the simple traumatic type of 
erythema, and the line of demarcation between the inflamed and normal 
areas presents a greater contrast. The pain is usually intense. In addition 
to the local manifestations, there are usually present fever, accelerated 
pulse, and other symptoms of systemic derangement. 

The treatment is that of facial erysipelas: Rest in bed, catharsis, 

97 


7 


98 


DISEASES OF THE EXTERNAL EAR 


tonics, local cleansing, application of antiseptic or antiphlogistic oint¬ 
ments or lotions. Many of the local measures advocated have seemed to 
the author to exert little or no influence on the course of the lesion, and, 
though recovery is the rule, one is not always sure to what extent this 
happ}^ result is due to the remedies applied. The writer is inclined to 
believe that for severe cases the use of a leucocyte extract (Hiss) will 
prove to be the treatment insuring the most definitely favorable results. 
In a later chapter dealing with serum therapy in the treatment of aural 
disease, the control of erysipelas by the Hiss leucocyte extract will be 
briefly discussed. 

Frost=bite. —The auricle from its exposed position is peculiarly vul¬ 
nerable to this accident. The symptoms are characteristic, but are often 
at the time overlooked by the sufferer. The ear, which has been tingling 
with cold, is suddenly found to be insensitive to touch. On examining 
the ear, the affected part of the auricle—oftenest the tip of the lobe or 
margin of the helix, or both—is found to be dead white and absolutely 
insensitive. The adjoining uninvolved part of the auricle is deep pink or 
red. Later—unless the circulation is quickly re-established—the frozen 
part becomes purplish, and still later may become dark brown or black, 
the part so discolored being afterward separated as a slough. This necro¬ 
sis may not involve the cartilage, but simply the superficial tissues. In 
still milder cases distinct sloughing does not take place, the parts gradually 
regaining tone and, after desquamation of the skin has taken place, re¬ 
turning to an apparently normal condition. That the tissues do not quickly 
return to an absolutely normal state is shown, however, by the fact that 
even in very mild cases the parts attacked are usually for a considerable 
period thereafter particularly vulnerable to the influence of cold, and there¬ 
fore to recurrence on comparatively slight exposure. 

Treatment. —The first indication is to re-establish the local circula¬ 
tion in the part frozen. Heat should not be applied, nor should the sufferer 
be taken into a warm house or room. If snow is on the ground, vigorous 
rubbing with snow, or better still with the hands after they have been 
made cold by contact with the snow, is a time-honored custom, and prob¬ 
ably the best method which can be employed. Restoration of the local 
circulation will be announced by the return of local sensation and pain. 
Later the ears must be carefully protected from renewed exposure, and, if 
it becomes evident that sloughing is to some extent inevitable, they should 
receive antiseptic care and treatment in accordance with the surgical laws 
governing the management of necrotic or gangrenous wounds. 

Auricular Eczema. —Clinically, eczema of the external ear is recog¬ 
nized in two clearly differentiated forms, the acute and the chronic. 

Etiology. —The acute form occurs far more frequently in childhood 
than in adult life, and in the uncared-for and ill-fed children of the tene¬ 
ments than among those living under more favorable hygienic conditions. 
Early childhood and depressed constitutional states must, therefore, be 
regarded as strongly predisposing factors. Digestive disturbances, and 
especially intestinal disorders, also seem to influence the development of 



AURICULAR ECZEMA 


99 


the disease. The chronic form is seen oftener in adult life and old age, 
and with particular frequency in those in whom the rheumatic or gouty 
diathesis is present. 

Symptoms of Acute Auricular Eczema. —Three stages of the lesion 
are frequently seen in aural clinics: (1) The erythematous stage, in which 
the skin is intact, but red, somewhat swollen and angry looking. (2) The 
vesicular stage, in which the skin is more or less covered with vesicles. 
From some of these serum exudes which bathes the inflamed surface, 
finally drying in the form of scales. (3) A stage in which the area involved 
is completely denuded of its epithelium and presents a raw and bleeding 
surface. 

The chief symptom is that of the very distressing local irritation,— i.e. 
the intolerable itching. This is present in all stages. In the erythematous 
stage there is sometimes in children very considerable pain, giving rise in 
some cases to moderate elevation of temperature. 

The parts most frequently involved are (1) the postauricular sulcus 
and contiguous parts behind the ear; and (2) the concha and often the 
outer half of the membrano-cartilaginous meatus. Children find it im¬ 
possible to resist the inclination to scratch the intensely itching surfaces, 
and this often adds a superficial infection to the primary lesion. 

Treatment. —Fortunately, these cases usually respond readily to 
proper management. The writer usually begins with internal remedies 
to cleanse the intestinal tract and regulate the digestion. For this pur¬ 
pose the following well-knowm formula for rhubarb and soda gives very 

satisfactory results: 

%/ 

R Extract, rhei fluid., 

Sodii bicarbonatis, 

Spirit, menth. piper., aa ^i; 

Aquae dest., q. s. ad ,$ iv. 

M. Sig.—One teaspoonful in wineglass of water t.i.d., a.c. 

The local treatment calls for cleanliness, application of an astringent 
ointment, and protection from mechanical irritation (scratching, etc.). 
The parts should be gently bathed with warm water and castile soap, 
and thoroughly dried. They should then be covered rather thickly with 
some soothing and astringent ointment. The parents should be instructed 
to reapply this ointment two or three times daily as may become necessary, 
and not again to bathe or apply water to the part until so instructed. 
The ointment which the writer is accustomed to prescribe is as follows: 

R Unguent, zinci oxid., 

Petrolati, aa ^ss. 

M. et ft. unguentum. 

When the skin is very acutely inflamed, much quicker and more satis¬ 
factory results are obtained by applying the ointment once daily and 
protecting the parts in the interim by means of a dressing of sterile gauze. 
It is surprising how rapidly and completely most cases of acute auricular 
eczema will clear up under this treatment if faithfully carried out. 


100 


DISEASES OF THE EXTERNAL EAR 


A condition the treatment of which presents some difficulties is found 
in cases in which acute eczema of the meatus and auricle coexist with 
discharge from the middle ear. In such cases the syringing employed to 
cleanse the canal of pus exerts an unfavorable influence upon the eczema. 
Under such circumstances the eczematous surfaces should be guarded 
from the irrigation fluid by thick layers of the protecting ointment. When 
the aural discharge is not profuse, manual cleansing and drying of the 
meatus, followed by the introduction of gauze wicks,—the whole ear 
being covered with a gauze dressing,—may with advantage be substituted 
for irrigation of the ear. Such a dressing would have to be renewed daily. 

Chronic eczema of the auricle usually involves also the outer half 
or third of the external auditory meatus. Two clearly distinguishable 
types are recognized: (1) The squamous variety, in which the outer part 
of the meatus and part of the concha are covered with dry, thin scales of 
exfoliated epithelium. Removal of these scales exposes a sensitive and 
easily irritated surface. (2) The so-called sclerotic type of eczema, in 
which the skin lining the outer part of the meatus and covering parts of the 
auricle is greatly thickened. The calibre of the meatus is in some cases 
greatly reduced by superposed layers of exfoliated epithelium, removal of 
which is apt to leave an excoriated and bleeding surface. In both types 
of chronic eczema, itching is usually a more or less prominent symptom, 
and the patient’s effort to relieve this by scratching tends to prolong and 
exaggerate the condition. 

Treatment. —Tonics and—in cases in which such a diathesis exists— 
antirheumatic remedies seem to influence some cases favorably. The 
local treatment calls for the removal of the scales, or exfoliated epithelial 
layers, lining the canal and concha. Unfortunately, this is often quite 
difficult or impossible without leaving a raw or abraded surface, which 
opens the door either to infection or to the formation of scabs or crusts, 
beneath which epithelial hyperplasia and exfoliation proceed as before. 
It is well, therefore, in some cases to apply an emollient ointment for 
several days before attempting to remove the thickened and adherent 
surface layer. For this purpose the following is quite satisfactory: 

R Glycerini, %i; 

Lanolini, ^iii; 

Unguenti petrolati, 5 i. 

M. et ft. unguentum. 

This should be applied thickly each day until the abnormal surface cov¬ 
ering of the canal is softened, and can be easily removed without injury 
to the underlying skin. The parts should then be thoroughly cleansed 
with 95 per cent, alcohol, and covered by some protective ointment,— 
e.g., the zinc oxide ointment, or the following: 

R Ichthyoli, 31 ; 

Acidi salicylici pulv., gr. x; 

Zinci oxidi, £ss; 

Unguent, aquae rosae, ^ i. 


AURICULAR PERICHONDRITIS 


101 


Later, occasional swabbing of the ear with alcohol helps to restore to 
the skin its normal tone. It must, however, be kept soft by frequent 
applications of some astringent ointment to prevent re-formation of the 
scales. The condition regularly improves under careful local treatment, 
but I know of nothing which will absolutely insure against recurrence after 
treatment has been discontinued. 

Auricular Perichondritis. —This is an inflammation involving the auric¬ 
ular perichondrium, and usually resulting in an effusion of pus or 
serum between it and the auricular cartilage. It is said in some cases to 
develop idiopathically, or at least without known cause (Politzer); but 
in the vast majority of cases it is traceable to a direct infection, spreading 
either from a neglected furuncle of the cartilaginous meatus, from a lace¬ 
rated wound of the auricle, or the infection may be traced to a plastic 
operation involving the cartilage,— e.g., the plastic work upon the carti¬ 
laginous meatus forming part of the “radical operation.” 

Symptoms. —The onset is announced by gradually increasing auricu¬ 
lar pain, which soon becomes exceedingly severe and usually interferes 
with sleep. Upon examination we find at the beginning a small area of 
localized swelling. The area involved is dark red or purplish red, is hard, 
tense, and unyielding to the palpating finger, and is exquisitely sensitive 
to manipulation or pressure. These changes may at first be confined to a 
very small area, from which they may spread gradually in all directions 
over the anterior surface to the extreme limits of the auricular cartilage. 
With the spread of the lesion, the tumefaction becomes less hard, impart¬ 
ing a boggy feeling to the palpating finger,—never that characteristic of 
fluctuation. Naturally the lobe is never involved, and this supplies a 
differential point between auricular perichondritis and a severe and exten¬ 
sive auricular inflammation of more superficial origin, in which the lobe is 
apt also to be involved. Fever and accompanying pulse changes are 
frequently present in some degree at the onset. 

Terminations. —(A) The lesion may undergo resolution with absorp¬ 
tion of pus or serum and a return to the normal. (B) There may be 
local recovery with considerable permanent thickening and deformity. 
(C) The presence and pressure of the pus may give rise to necrosis of the 

cartilage, with very great permanent deformity. 

Treatment.— The treatment varies with the severity and extent of 
the lesion, and calls for the surgeon’s best judgment. When the disease 
is apparently localized in a small area and shows no tendency to spread, 
the application of a wet dressing,— i.e., of a saturated boric acid solution 
as hot as the patient can bear, and renewed frequently, or of a 10 per 
cent, solution of ichthyol, may help to control the inflammation. W hen, 
however, a considerable effusion of fluid has taken place beneath the 
perichondrium, it is safer to sterilize the part as for a major operation and, 
with the patient under a general anaesthetic, make a free incision through 
the perichondrium. After the fluid has been evacuated, a ver\ small 
gauze drain should be introduced into the wound and for a short distance 


102 


DISEASES OF THE EXTERNAL EAR 


between the cartilage and perichondrium, and over this pressure applied 
by means of a pad of sterile gauze, this being reinforced by a larger gauze 
dressing. This dressing should be changed daily, and particular care 
taken to prevent reaccumulation of serum or pus beneath the perichon¬ 
drium. If this operation is unduly delayed, more radical measures may 
become necessary through necrosis of the cartilage. 

So long as the inflammation is confined to the perichondrium— i.e ., 
so long as the cartilage is not directly involved—through-and-through 
drainage by an incision passing through the auricular cartilage is not called 
for. Very great swelling of the auricle is often seen as a result of inflam¬ 
matory infiltration of the perichondrium plus an effusion of fluid between it 



Fig. 80. —Auricular perichondritis. Fig. 81.—Deformity resulting from neglect of lesion 

shown in Fig. 80. 


and the cartilaginous plate. In such cases incision of the cartilage does 
not seem called for. If, however, after incision of the perichondrium, the 
exposed cartilage is found to have become involved and to have undergone 
necrosis, there should be no delay in dissecting from it its perichondrial 
covering and exsecting the necrotic area. Unless this is done promptly, 
the whole cartilaginous frame may become necrotic, with ultimate very 
unpleasant permanent deformity. 

Haematoma Auris (Othaematoma). — This describes a condition in 
which, as a result of local injury, there has occurred an effusion of blood 
between the auricular cartilage and its perichondrium. It occurs only on 
the anterior surface of the cartilage. At first usually localized, it may 
spread later so as to separate the perichondrium from the entire anterior 
surface of the auricular cartilage. 

Etiology. —This is somewhat obscure. Apparently the aged and more 
especially the insane are particularly prone to certain degenerative changes 
in the auricular cartilage and perichondrium, in which condition haematoma 
auris is apparently easily induced by very slight injuries. Its occurrence 




HiEMATOMA AURIS 


103 


in this class of individuals has been noted with particular frequency in 
Germany, and the occurrence there of certain cases in which no history 
of trauma could be obtained has led to the belief that a certain number 
of cases occur spontaneously. One wonders, however, whether even in 
such cases—depending unquestionably in some degree upon degenerative 
tissue changes—there has not been some slight injury which, though over¬ 
looked at the time, has been the directly exciting cause. In this country, 
so far as the writer knows, the condition is almost always due to direct 
violence. In twelve years of almost daily 
attendance at aural clinics and hospital wards, 
no single case has come under his observation 
which could not be directly traced to local 
injury. The commonest cause is a fist blow 
on the ear, but it has occurred also as the re¬ 
sult of a hard slap and of violent twisting or 
pulling of the ear. The accompanying illus¬ 
tration is of a prize-fighter in whom the lesion 
resulted from a blow (Fig. 82). 

Symptoms. —Following the injury, a tumor 
upon the anterior surface of the auricle is 
rapidly formed. At first localized, it may 
spread rapidly upward and backward to the 
helix, and downward to the upper boundary 
of the lobe. The tumor is generally purplish 
or bluish red, its local temperature is usually 
elevated, and it presents the peculiar boggy feeling characteristic of fluid 
confined beneath the perichondrium. If very small and localized, the 
pain may not be severe. With an effusion of considerable size, the pain 
is usually intense. Insomnia due to pain, fever, and constitutional 
depression is apt to be present in severe cases. 

Terminations. — (1) With a small effusion there may be complete 
and perfect local recovery. (2) The lesion may undergo resolution, part 
of the blood being absorbed and the remainder being organized into new 
connective tissue, which results in permanent thickening and deformity 
(Fig. 83). (3) Infection may occur, giving rise to destruction of the car¬ 

tilage, and ending in final recovery with great permanent deformity. 

Treatment. —When the collection of blood is small, shows no ten¬ 
dency to increase, and is not accompanied by excessive pain, it is well to 
depend largely upon time to bring about a cure. From the nature of the 
lesion, it is difficult to see how the application of lotions can be of value, 
and pressure or manipulation may obviously do harm. 

In the case of a large effusion of blood, the indications for treatment are 
well suggested by the statement of Richard Lake, of London, that spon¬ 
taneous recovery “is not certain to take place, but if it does, deformity is 
sure to result.” In such a case a free incision—coextensive with the extent 
of the effusion—should be made through the perichondrium. A puncture is 





104 


DISEASES OF THE EXTERNAL EAR 


worse than useless. The blood or coagulum should then be evacuated, a 
curette if necessary being used for the removal of firmly organized clot, 
and the space between perichondrium and cartilage should be lightly 
packed with sterile gauze. This dressing should be changed daily for 
several days, after which it may be omitted, and the parts pressed into 
apposition and held so by a gauze pad and dressing. If, as advised by 
some surgeons, the cavity is not packed, but is at once subjected to pressure, 
reaccumulation of blood is more than likely to occur. 

Differential Points between Auricular Perichondritis and Haematoma 
Auris .—While the two lesions present clinically many similar features, 
they may usually be differentiated by consideration of the following 
points: (A) History: Auricular perichondritis is usually traceable to a 

localized point of infection,— e.g., fur¬ 
uncle, lacerated wound, plastic surgery 
involving the perichondrium. Hsema- 
toma auris is usually traceable to direct 
violence,— e.g., a blow. (B) Rapidity 
of development: Following a local infec¬ 
tion, the development of auricular peri¬ 
chondritis is comparatively gradual and 
slow. Following an injury, the develop¬ 
ment of haematoma auris is exceedingly 
rapid. (C) Auricular perichondritis un¬ 
der transillumination shows no marked 
color differences between involved and 
uninvolved areas. In haematoma* auris 
transillumination gives a dark purplish 
color over the area of the blood collection 
or clot. 

Lupus. — Tubercular lesions of the 
skin covering the auricle, while probably 
fairly common in dermatological practice and clinics, do not come very 
often before the aurist. Only in cases giving rise to considerable swelling 
and deformity of the auricle (lupus hypertrophicus, lupus tumidus) is the 
aurist likety to be called in. The student will, therefore, find more 
authentic descriptions and directions for treatment of these lesions in 
works on dermatology. 

The commonest form (lupus vulgaris), when attacking the auricle is 
usually seen simultaneously upon other parts of the face. The lesions 
appear as distinct papules or tubercles, reddish or brownish in color, 
which may later be covered with dry, brownish scales. A characteristic 
feature is the tendency to form permanent depressions, the substance of 
the tubercles apparently in some cases being absorbed or shrinking with¬ 
out erosion of the overlying skin. Between these depressions are often 
formed small cicatrix-like bands. The disease is distinguishable from a 
syphilitic skin lesion of somewhat similar appearance (a) by absence of 







Plate V. 



Fig. 84.—Lupus hypertrophicus auriculae 














SYPHILIS OF THE EAR 


105 


a history or evidence of syphilitic infection, (b) by their slower develop¬ 
ment, and (c) by the greater tendency of the syphilitic papules to ulceration. 

Treatment. —The treatment calls for constitutional building up of 
the patient by constructive tonics. The local treatment aims at the actual 
destruction of the diseased tissue forming the basis of each tubercular 
nodule. For this purpose, the nitrate of silver stick, the sharpened point 
of which is forced down into the core of each nodule, is said to be effective. 
Actual surgical removal of the tubercles, the denuded surface being later 
covered by skin-grafts, is also recommended. The skilful local use of 
the X-ray is said also to exert a curative action on tubercular skin lesions. 

Lupus Tumidus (Lupus Hypertrophicus). — According to Politzer, 
this form of tubercular lesion may result by the following process from 
the more common variety (lupus vulgaris). The typical superficial tuber¬ 
cles, or nodules, becoming confluent, undergo surface necrosis, giving rise 
to a tubercular ulcer. Within the depths of this ulcerated surface are 
deposited newly formed tubercular nodules. Following this there is a 
moderate proliferation of firm granulations which bleed easily. This may 
result in great thickening or enlargement of the involved portion of the 
auricle, which usually includes the lobule. The accompanying illustra¬ 
tion (Fig. 84) represents a lesion of this nature. Unless brought under 
fairly prompt control, the cartilage may become involved, and, should it 
undergo necrosis, great permanent deformity is likely to result. 

In rare cases a tubercular lesion of the auricle assumes the form of a 
tumor of considerable size. Tubercular lesions of this form involving the 
auricle are apparently much commoner in certain parts of Europe than in 

this country. 

Treatment. —The treatment recommended for this lesion is prompt 
and thorough removal of the diseased tissue. The tubercular granulations 
and nodules are subjected to vigorous curettage with a sharp spoon curette 
until healthy tissue is reached. This surface should then be painted with a 
strong solution of silver nitrate, 200 grains to the ounce, in order to destroy 
such tubercular tissue as the curette has failed to remove. The parts are 
then dried and covered with a protective gauze dressing. The above 
treatment may have to be repeated several times before the disease is 
eradicated. Finally skin-grafting may be practised in order to hasten 
the healing process and lessen cicatricial contraction. In severe lesions 
some deformitv is probably inevitable, but is less than if the lesion is 
allowed to involve the cartilage before treatment is instituted. 

Syphilis of the Ear. —Primary syphilitic lesions of the auricle, while 
a few cases have been recorded, are exceedingly rare. The writer in twelve 
years of attendance in aural clinics and hospitals has not met with a 
single case. Secondary lesions, however, in the form of papular or 
pustular eruptions, coincident with similar lesions upon the scalp, fore¬ 
head, or other parts of the body, are said to be of fairly common occurrence 

in dermatological clinics. 

The severe lesions— i.e., deep ulcerations and condylomata are more 


106 


DISEASES OF THE EXTERNAL EAR 


often seen within the meatus. While the physical appearances may be 
most suggestive, their specific character can be positively determined only 
by the association of a reliable history of syphilitic infection, tne presence 
of other evidences of constitutional syphilis, or possibly by a positive 
Wassermann reaction. The condylomata are described as “ grayish-red, 
ragged, watery excrescences,” firmer than the ordinary form of inflam¬ 
matory granulation tissue, and tending to spread with great rapidity. 

The formation of gummata upon the auricle or within the meatus is 
said to be exceedingly rare. 

A final and confirmatory diagnostic test of these lesions is found in 
their response to antisyphilitic treatment. 

The treatment is constitutional rather than local. The local treatment 
aims chiefly at cleanliness. The chief reliance, however, is to be placed 
upon the constitutional remedies. Mercurial injections or inunctions with 
potassium iodide in appropriate doses usually exert a fairly rapid influence 
upon the local lesion. Salvarsan is even more rapid and positive in its 
results. Probably the best results will be obtained by fairly large and 
repeated injections of salvarsan in combination with some form of mer¬ 
curial medication. For a general consideration of the value of salvarsan 
in aural therapy the reader is referred to a later chapter dealing particu¬ 
larly with the influence of that drug upon labyrinthine and auditory nerve 
lesions. 

Herpes Zoster Auriculae; Herpetic Inflammation of the Geniculate 
Ganglion (Hunt). —The occasional appearance of herpes upon the auricle, 
with the coincidence of aural symptoms of varying severity, has long 
been known to occur, but only since the publication of Dr. J. Ramsay 
Hunt’s papers on the subject have we possessed any definite con¬ 
ception of the nature of the lesion. We now recognize the symptoms as 
directly due to an inflammation of the geniculate ganglion. According 
to Hunt, the zoster zone of the geniculate ganglion is sharply confined to 
the membrana tympani, the walls of the auditory meatus, the concha, 
tragus, antitragus, antihelix, and helix, rarely extending beyond the 
boundaries of this area. The herpetic eruption (Fig. 85) may occupy the 
whole or only a small portion of the geniculate zone. The appearance 
of the herpes is occasionally preceded by rather severe pain referred to 
the ear and mastoid region. With the development of the herpes there may 
be considerable swelling of the canal and pinna. 

The symptoms may be limited to the aural pain; or the inflammation 
may spread from the ganglion to auditory and facial nerves, in which case 
there may be marked disturbance of hearing (cochlear branches of 8th 
nerve,) or symptoms of vestibular irritation,— i.e., nystagmus, vertigo, 
vomiting, etc. The latter phenomena point of course to involvement of 
the vestibular branches of the 8th nerve. Since the connection of the 
geniculate ganglion with the 7th nerve is far more direct and intimate then 
with the 8th nerve, facial paralysis is far more frequent than are the symp¬ 
toms due to disturbances of the 8th nerve, with which the geniculate 





ACUTE CIRCUMSCRIBED EXTERNAL OTITIS 


107 


ganglion communicates chiefly through the small connecting branch known 
as the pars intermedia. 

It is of the greatest practical importance that aurists should be pre¬ 
pared to recognize this lesion, for the reason that in a severe case the 
physical signs may strongly resemble those of a severe tympano-mastoid 
inflammation, in which rupture of the drum-head has not occurred. 

The history of aural pain, quickly followed by herpes confined to the 
geniculate zone and the frequent occurrence of paresis or paralysis of the 
muscles supplied by the facial nerve, should enable the careful observer to 
arrive at a correct diagnosis. A careful reading of the papers referred to 
below is advised. 1 - 2 

Malignant Disease of the Auricle: Epithelioma; Cancer of the 
Auricle. —Epithelioma of the auricle is not very common and, when it 
does occur, shows no distinctive features directly attributable to its situa¬ 
tion. That is to say, it presents the characteristic features common to 
such growths in whatever region they may appear. Epithelioma origi¬ 
nating at some point upon the auricle grows rapidly, and the overling 
skin is quickly eroded. The auricular cartilage is soon involved and may 
be very rapidly destroyed. 

As to the surgeon’s responsibility in the management of these cases, 
there is one point which can not be too strongly emphasized, viz., that 
an epithelioma originating upon the auricle may in the first stage be re¬ 
moved surgically with good chances of a permanent cure. If surgical 
relief is long withheld, however, the neoplasm may suddenly exhibit very 
rapid growth, spreading quickly through the auditory canal to the tym¬ 
panum, to the parts in front of and behind the ear, and finally may attack 
and destroy a large portion of the temporal bone. When such extensive 
involvement has taken place, recurrence is likely to follow any operation 
which may be employed. 

INFLAMMATORY DISEASES OF THE EXTERNAL AUDITORY MEATUS. 

Acute Circumscribed External Otitis; Furunculosis of the Meatus — 
A furuncle in the meatus is one of the most painful, as it may be one of the 
most troublesome, conditions which the aurist is called upon to treat. It in¬ 
volves only the outer, or fibrocartilaginous, portion of the canal. It may 
be single or multiple. It occurs most frequently upon the posterior wall 
or floor, next upon the roof, and least frequently on the anterior wall. 

Etiology. —Predisposing Causes .—The number of cases in which the 
same person in different years has suffered from recurrent furuncles of the 
meatus, and the still greater tendency of the lesion to immediate recur¬ 
rence, impel one to believe that there are certain predisposing factors 
net always easy to determine—which render certain individuals pecu- 

1 Hunt, J. R.: Herpetic Inflammation of the Geniculate Ganglion; Jour, of Nervous 
and Mental Diseases, February, 1907. 

2 Hunt, J. R.: Further Contribution to Inflammations of the Geniculate Ganglion; 
Amer. Jour, of the Medical Sciences, August, 1908. 






108 


DISEASES OF THE EXTERNAL EAR 


liarly susceptible to the disease. People, for example, having the gouty or 
rheumatic diathesis seem to be particularly frequent sufferers. Depressed 
constitutional states — e.g ., lowered vitality caused by insufficient food or 
unhealthful surroundings or modes of life—are undoubtedly factors,, as 
is shown by the relative frequency of furuncles of the meatus among the 
poorer class of dispensary patients as compared with those seen in private 
practice. It occurs, however, in all classes. Chronic eczematous affections 
of the concha or meatus also predispose to the development of furuncles, 
probably by affording denuded points for the entrance of germs. 

The exciting cause is always a local infection. This may be brought 
about by a chronic purulent discharge from the middle ear acting upon a 
denuded area in the meatus. Quite often the lesion may be traced to the 
habit of scratching the canal wall with a toothpick, hairpin, or even w T ith 
the finger-nail, this resulting in an abrasion which provides the point of 
entrance for infective matter. 

Symptoms. —The symptoms of which the patient complains may be 
mentioned in the following order: (a) Sensitiveness to slight manipula¬ 
tion; (b) pain; (c) tinnitus aurium; (d) impairment of hearing. Discharge, 
when present, occurs so late in the disease, and is so frequently absent, 
that it can hardly be regarded as a characteristic sj^mptom. 

The patient may first be conscious of a sense of occlusion, or “ stuffi¬ 
ness,” in the affected ear, and with this he may notice that very slight 
manipulation— e.g., as in drying the ear after the morning bath—gives 
rise to a sense of soreness or even a sharp pain in the ear. Later this dis¬ 
comfort or pain may be induced by extensive movements of the jaw, as in 
yawming. The next symptom is usually that of constant pain in the ear, 
at first of moderate grade, but gradually increasing and finally becoming 
unbearably severe. The pain caused by a furuncle of the meatus is in many 
cases quite as severe as that accompanying acute otitis media, and is 
augmented by the intolerable sense of soreness usually present. A charac¬ 
teristic feature of this pain is found in the fact that it is usually made 
worse by movements of the jaw,— e.g., chewing, yawning, etc. This is, 
of course, explained by the close anatomical relation of the cartilage of the 
temporomaxillary joint and the cartilaginous framework of the meatus. 
This phenomenon, when present, is pathognomonic either of acute cir¬ 
cumscribed or acute diffuse external otitis, and clearly differentiates these 
lesions from acute inflammatory conditions confined to the middle ear. 
Tinnitus aurium is a symptom the prominence of winch varies in differ¬ 
ent cases from slight head noises, that are overlooked in the severity of 
other symptoms, to loud ringing noises which add much to the patient's 
discomfort. In some degree it is nearly always present. Impairment of 
hearing is not usually present at the onset, but becomes progressively 
more noticeable as the calibre of the canal is reduced, and may be very 
marked if the occlusion of the canal is complete. 

Physical Examination. —Palpation comes first as a means of deter¬ 
mining the presence of a furuncle in the meatus, for the reason that it will 


ACUTE CIRCUMSCRIBED EXTERNAL OTITIS 


109 


in many cases elicit tenderness before changes in the contour and color 
of the canal wall can be detected. The finger should be pressed firmly 
against the cheek above and in front of the auricle, and brought downward 
along the line of anterior attachment so as to press the tragus inward. 
This will surely elicit tenderness if there is a furuncle in the anterior canal 
wall, and often even though it may be situated elsewhere in the fibrocarti¬ 
laginous meatus. If, however, no pain is caused by pressure on the tragus, 
the cartilaginous meatus should be moved in different directions,—i.e., 
forward, upward, and downward. If this procedure causes no pain, we 
may be quite confident that the disease is not located in the fibrocarti¬ 
laginous canal. 

Inspection by Reflected Light. —In the earliest stage of a furuncle in 
the canal, inspection may not reveal any localized swelling nor any changes 
in the color of the overlying skin. In this case the different walls of the 
canal should be subjected to pressure by means of a cotton applicator 
wound with cotton. In this way we are usually able to determine the point 
of local tenderness, which coincides, of course, with the point of infection. 
Later, inspection will reveal one or more points of localized swelling, 
according to whether we have to deal with a single furuncle or with a mul¬ 
tiple lesion, furunculosis. With the progress of the lesion the canal is always, 
therefore, narrowed in one or more of its diameters, in accordance with 
the involvement of the different walls. In severe cases the swelling may be 
so great as completely to close the canal. Even in such cases, however, 
it may be possible to introduce a very small speculum beyond the furuncle 
and thus bring the drum membrane into view. Whenever possible with¬ 
out the infliction of too much suffering, this should be done. Careful 
inspection of the drum membrane is important for the reason that, as 
soon as we can determine that the membrana tympani is not acutely 
inflamed, we are in a position to exclude positively the middle ear as the 
site of intercurrent suppurative inflammation, and this without inspect¬ 
ing the drum membrane we are not able to do. 

Course of the Disease. —In some cases a single furuncle will rupture 
spontaneously into the canal, and this may, or may not, determine a 
favorable course toward recovery. Oftener than not, such spontaneous 
rupture does not provide adequate drainage, and the inflammatory proc¬ 
ess continues to spread, foci of infection (i.e., furuncles) developing 
simultaneously upon other walls of the canal. Quite frequently sponta¬ 
neous rupture is so long delayed as to cause the patient excruciating pain, 
the inflammation finally extending to surrounding structures. 

Extensions of Inflammation. —The involvement of structures about 
the ear depends somewhat upon the site of the furuncle. (A) With a 
furuncle upon the anterior wall, there often occurs very marked swelling 
of the tissues in front of and below the tragus. In such cases the parotid 
gland may be distinctly involved. (B) With a furuncle confined to the 
posterior or posterosuperior canal wall, there is not infrequently very con¬ 
siderable oedema over the mastoid region immediately behind the ear. 


110 


DISEASES OF THE EXTERNAL EAR 


This commonly results in more or less complete obliteration of the post- 
auricular sulcus and the production of a very characteristic deformity,—— 
the auricle being displaced forward, or forward and downward, so that it 
stands out from the head in striking contrast with the opposite sound ear 

(Fig. 86). 

Extension of inflammation may also take place through the deeper 
structures of the auricle itself,— i.e., it may cease to be in any sense a 
circumscribed inflammation, and spread widely between the perichondrium 
and cartilage, giving rise to severe and extensive suppurative perichon¬ 
dritis (Fig. 87). 



Fig. 86.—Displacement of left auricle resulting from 
a furuncle in the posterosuperior canal wall. 



Fig. 87.—Necrosis of auricular cartilage and 
deformity resulting from extension of infection 
from a furuncle in the canal. (Dr. Held’s 
case.) 


With a severe infection of the fibrocartilaginous canal, it is not unusual 
to find the lymphatic glands of the neck, particularly those in front of 
and behind the sternomastoid muscle of the affected side, enlarged and 
somewhat sensitive to pressure. 

Since swelling behind the ear with consequent displacement of the 
auricle may occur with acute suppurative mastoiditis as well as with 
furunculosis of the meatus, it may be well to mention here three points 
which should aid us in differentiating between the two conditions causing 
this deformity: 


Postauricular (Edema due to Furuncle 
of the Meatus. 

1. Drum membrane usually intact, 
and may be normal or only slightly con¬ 
gested. 

2. Pressure upon tragus and manip¬ 
ulation of auricle causing movement of 
fibrocartilaginous meatus usually cause 
severe pain. 


Postauricular Swelling due to Acute 
Suppurative Mastoiditis. 

1. Drum membrane usually perforated, 
and always shows some of the cardinal 
signs of suppurative otitis media. 

2. Pressure upon tragus and manipu¬ 
lation or movement of fibrocartilaginous 
canal cause absolutely no pain. 










ACUTE CIRCUMSCRIBED EXTERNAL OTITIS 


111 


3. Firm pressure over the mastoid 
process just behind the postauricular sul¬ 
cus and opposite the orifice of the meatus 
will, if so directed as not to disturb the 
position of the auricle, cause absolutely 
no pain. The cedematous tissues pit 
deeply under the compressing finger, after 
which no bone tenderness can be elicited. 
Pressure at exactly the same point, but 
directed slightly forward so as to disturb 
the auricle, causes severe pain. 


3. Firm pressure upon the mastoid 
process just behind the postauricular sul¬ 
cus and opposite the orifice of the meatus 
usually elicits deep-seated bone tenderness. 


The practical diagnostic value of the above is well illustrated by the 
following case. The author was asked by a general surgeon to confirm a 
diagnosis of mastoiditis in a hospital patient upon whom he was about to 
operate. The patient, a man of thirty years, presented superficially the 
following conditions, upon which the diagnosis had been based: (1) he was 
suffering severe earache; (2) there was very marked oedema behind the 
left ear and the postauricular sulcus was obliterated; (3) the auricle was 
displaced forward and stood out from the side of the head in conspicuous 
contrast with its fellow of the opposite side. The parts about the ear were 
shaved in preparation for immediate operation. That the mastoid was 
not involved was clearly shown by the following facts: (a) the drum mem¬ 
brane, rather difficult to inspect, was found to be practically normal; 
(b) the posterior wall of the fibrocartilaginous meatus was intensely in¬ 
flamed ; (c) any manipulation of the auricle causing movement of the carti¬ 
laginous meatus caused intense pain; (d) firm pressure upon the mastoid, 
so directed as not to disturb the auricle, caused the patient no pain. I 
learned later that he made a perfect recovery under treatment appropri¬ 
ate to furunculosis of the meatus. 

Prognosis. —The prognosis in this lesion is somewhat clouded by the 
pronounced tendency to recurrence. A single furuncle may appear to be 
progressing favorably toward recovery, only to be succeeded by a second 
furuncle on the opposite wall of the canal. Every aurist can recall cases 
in which the patient has been afflicted with a series of furuncles,—three, 
four, five, or more,—each following the other in the same canal and in 
rather quick succession. It is well, therefore, to acquaint the patient with 
this danger, and impress upon him the importance of following the pre¬ 
scribed treatment to the letter. 

Treatment. —The marked tendency to recurrence would seem to 
prove a constitutional basis in many of these cases. Internal, or constitu¬ 
tional, remedies should, therefore, play some part in their management. 
The treatment in every case should begin with thorough cleansing of the 
alimentary tract. Further than this, it is well to divide these cases into 
two general classes,— i.c., (1) those presenting evidences of lowered vitality 
or resistance, for whom simple or constructive tonics should be prescribed; 
and (2) the overfed, full-blooded, or plethoric class, the type of individ¬ 
ual to whom in the older text-books the term 1 apoplectic was applied. 
Such an individual requires careful regulation of diet, restriction of alco- 


112 


DISEASES OF THE EXTERNAL EAR 


holic drinks, and regulation of the bowels. For the latter purpose the 
administration of small doses of rhubarb and soda three times a day before 
meals has proved very satisfactory. This rather empirical method of 
classifying and prescribing for patients suffering from furunculosis of the 
meatus, has seemed favorably to influence the average results. 

That the local treatment of this lesion has proved a troublesome prob¬ 
lem in otology is shown by the long list of unrelated therapeutic measures 
which have been proposed for its relief. Many of these remedies have 
travelled a long journey, passing through one text-book to another, but 
have found little place in actual practice. Among them we find the fol¬ 
lowing: Abstraction of blood by the application of leeches in front of the 
tragus; abstraction of blood by the so-called artificial leech; application 
of heat (a) by means of poultices and (b) by fomentations,— i.e., applica¬ 
tion of heated lotions; application of cold by means of the Leiter coil; 
introduction into the meatus of various antiphlogistic agents, among which 
is mentioned pig’s fat impregnated with opium (Politzer), etc., etc. The 
writer believes that most of these remedies are worse than useless, and that 
we but obscure our view of the therapeutic field when we allow our atten¬ 
tion to be diverted from the few tried therapeutic measures upon which 
practical experience has stamped her approval. 

As the local treatment must necessarily vary with the condition pres¬ 
ent, it may be well to re-state briefly the four stages through which a 
furuncle may pass,—viz.: 

(1) Initial stage , in which the patient experiences a constant sense 
of discomfort, but pain only on manipulation of the cartilaginous meatus. 
Inspection may reveal no noticeable change in the contour or color of the 
canal, but palpation with a cotton-wound applicator discloses a point of 
maximum tenderness, representing the focus of infection. 

(2) Stage of inflammatory infiltration, in which inspection reveals circum¬ 
scribed redness and swelling of one or more walls of the meatus. Palpation 
shows the tumefaction to be hard, tense, non-fluctuating, and exquisitely 
sensitive to pressure. This is the most painful stage of the disease. 

(3) Abscess Stage. —The involved area, representing a circumscribed 
and encapsulated collection of pus, bulges into the canal, is found by 
palpation to be distinctly fluctuating, and may point and rupture spon¬ 
taneously into the canal. 

(4) Stage of Surrounding Cellulitis. —Certain cases fail to develop an 
encapsulated abscess, and extend by invasion of surrounding structures, 
giving rise to oedema or cellulitis in front of or behind the ear, with con¬ 
sequent displacement of the auricle. 

Local Treatment. —In the initial stage our purpose should be to abort 
the attack. The entire canal should be thoroughly cleansed of cerumen, 
exfoliated epithelium, or other impurities. This may be done by first 
irrigating the canal with warm boric acid solution and then scrubbing it 
out by means of cotton-wound applicators dipped in 95 per cent, alcohol. 
After this a pledget of cotton saturated with a solution of carbolic acid, 


ACUTE CIRCUMSCRIBED EXTERNAL OTITIS 


113 


Acid carbolic. gr. i 

Sodii bicarbonat. gr. xx 

Glycerin. 5 i 

Aquae, q. ad. 5i 






1 to 100 , should be placed in the meatus and allowed to remain for a min¬ 
ute, or until the part begins to tingle. This should leave the canal surgi¬ 
cally clean. As a permanent dressing my preference is for a wick of sterile 
gauze which has been saturated with a carbolic acid solution, 1 in 300, and 
then wrung out nearly dry. This should be packed rather a b 
firmly into the outer (membrano-cartilaginous) part of the 
canal, the pressure thus maintained seeming to influence 
these cases favorably. The concha should be filled with a 
ball of sterile absorbent cotton, which may be held in 
place by collodion or adhesive plasters. This dressing 7 
should be changed daily, the canal each time being thoroughly 
cleansed and dried. This method of treatment seems in a fair 
proportion of cases to have the effect of dispersing a beginning 
infection and bringing about a cure. When, however, this 
happy result does not follow, the lesion passes into the second 
stage, and may demand more vigorous measures for its relief. 

Second Stage .—In this stage the lesion is theoretically a 
surgical condition for which a free incision would seem the 
logical procedure, and this indeed may be ultimately necessary 
in any case reaching the stage of inflammatory infiltration. 

It is definitely established by experience, however, that a cer¬ 
tain considerable proportion of cases are controlled, and re¬ 
cover perfectly, under the following simple plan of treatment. 

The canal is cleansed as described in the last section, or simply 
by irrigation with a warm boric acid solution. A fold wick of 
sterile gauze, moistened in some non-irritating solution, is 
introduced into the canal, not tightly, and cut off so as not to 
protrude beyond the orifice of the canal into the concha. This 
wick is to be kept moist (not soaked) by some bland antiseptic 
solution. For this purpose the proprietary preparation, Cre- 
satin, gives excellent results. If this cannot be obtained, the 
following prescription has proved satisfactory in many cases: 


P 


y 


Fig. 88.—Furuncle 
knife. 


The wick should be kept moist by adding only three or four drops 
by means of a medicine dropper every two hours or so, a ball or pledget 
of sterile cotton being placed lightly in the concha in the intervals. 
Under this treatment the inflammation and infection is in many cases 
seen rapidly or at least progressively to subside. If too much of the solu¬ 
tion is used, so as to keep the wick soaked, maceration of the cutaneous 
covering of the canal is likely to occur, causing desquamation of the cuticle, 
with the added lesion of a diffuse and troublesome dermatitis. As soon as 
8 



















114 


DISEASES OF THE EXTERNAL EAR 


the localized infection is controlled by the above means, it is better to dis¬ 
continue the solution, merely keeping the canal lightly packed with a dry 
wick of sterile gauze for a few days. 

If the treatment above outlined fails to control the infection, and 
particularly if the inflammation is seen to be progressive, a free incision 
becomes the most rational step toward relief. As this operation, though 
short, is exceedingly painful, it is always best to have the patient under 
nitrous oxide anaesthesia. The canal should be previously sterilized by 
peroxide of hydrogen, followed by irrigation with a warm solution of car¬ 
bolic acid, 1 to 200. The point, or focus, of infection having been deter¬ 
mined by inspection and palpation, the knife should be introduced into the 
canal beyond the inflamed area, and the furuncle freely and rather deeply 
incised as the blade is withdrawn. For this purpose a straight knife (Fig. 
88) has always seemed to me more easily controlled, and therefore preferable 
to the curved bistoury frequently employed. While from the nature of the 
lesion the depth of the incision cannot be exactly gauged, our purpose 
should be (1) to have it so placed as to reach the centre of infection, and 
(2) to carry it through the inflamed cellular tissue and into the perichon¬ 
drium without cutting deeply into the cartilage. It is, however, better to 
cut a little too deeply rather than to err in the other direction with an 
incision too suoeificial to reach the source of trouble. An additional and 

X. 

important advantage of having the patient under the influence of an 
anaesthetic is that it permits one to use pressure for the removal of pus, 
should it be present, or at least to make sure by the use of a probe that the 
incision is sufficiently deep. 

After the patient recovers consciousness, which with nitrous oxide 
anaesthesia occurs within a few moments, it is well to irrigate the canal 
again with a carbolic acid solution, 1 in 200, as hot as the patient can bear 
it without too great discomfort. This second irrigation is distinctly useful, 
as the heat and the locally anaesthetizing effect of the carbolic acid reduce 
the sensitiveness of the part and facilitate the subsequent treatment. The 
canal should now be dried as thoroughly as possible and subjected to rather 
firm pressure by the introduction of a wick of sterile gauze which has been 
saturated with cresatin or a weak carbolic acid solution, 1 in 300, and 
then wrung out nearly dry. If such a patient can be confined to bed for 
a day or two, the efficacy of this treatment is likely to be enhanced, and in 
this case it is well to protect the ear with a large dressing of sterile gauze 
held in place by a bandage. The whole dressing should, of course, be 
changed daily. 

With regard to the irrigation fluid to be employed in cases of furuncu¬ 
losis, the writer believes that bichloride of mercury, even in weak solutions, 
should never be used, since it is likely to produce a dermatitis distinctly 
favorable to the development of secondary furuncles. If for any reason 
the use of carbolic acid is not advisable, a boric acid solution is non-irritat¬ 
ing and usually quite satisfactory. It is hardly necessary to state that 
carbolic acid in any solution stronger than that indicated in the prescription 


ACUTE CIRCUMSCRIBED EXTERNAL OTITIS 


115 


on the foregoing page should never be advocated for home use by the pa¬ 
tient or his family. 

The practice of incising a furuncle, and then directing the patient to 
syringe the ear at stated intervals, is quite unsurgical, the residual water 
left in the meatus being apt to macerate the skin covering the healthy 
portions of the canal, a condition distinctly favorable to the growth of 
bacteria. Cases so treated will be found to result in a large percentage 
of recurrences, whereas in my experience immediate recurrence is not 
frequent when the dry treatment, as above described, is carefully carried 
out. Routine irrigation of the ears is admissible only in one class of 
patients suffering from furunculosis of the meatus,—viz., dispensary 
patients who can be seen only at such loqg intervals that no other 
method is available. In such cases the best results will probably be 
obtained by prolonged irrigation, frequently repeated, with sterile water 
as hot as the patient can bear it. In advising hot irrigations, the patient 
should be informed that he will be likely with each repetition to experi¬ 
ence distressing vertigo, but that this discomfort will be short-lived and 
without serious consequences. 

Third Stage .—When a distinctly fluctuating abscess has formed at the 
site of the initial infection, the lesion is often no longer excessively painful, 
and incision usually causes much less pain than in the second stage. Never¬ 
theless, it is better, when practicable, to anesthetize the patient, so that 
following the incision the pus may be thoroughly expressed and the interior 
of the cavity scraped out, if need be, by means of a small curette, or swabbed 
out with a carbolic acid solution, 1 in 20. A small drain may then be intro¬ 
duced into the abscess cavity, and pressure applied by means of a wick of 
sterile gauze. 

In the fourth stage the treatment does not differ materially from that 
above described. It is very rarely necessary to incise the cedematous parts 
behind or in front of the ear, secondary abscesses in these regions being 
exceedingly rare. Incision at the point of infection in the canal usually 
relieves tension and provides an adequate pathway for the escape of pus. 
The application of a wet dressing over the adhacent cedematous areas may, 
however, prove of value. 

In the foregoing pages the author has outlined the plan of local treat¬ 
ment which in his own experience has seemed to insure the best average 
results. The best plan of local treatment, however, leaves the patient 
who has suffered from this painful and depleting lesion particularly prone 
to recurrences. 

Against these recurrences I believe that the patient’s most effective 
defense will be found in the use of an appropriate vaccine. Naturally, 
whenever pus from the lesion can be obtained, an autoginous vaccine should 
be prepared. Under present methods, however, the great majority of cases 
of furunculosis of the canal are controlled without incision. 


116 DISEASES OF THE EXTERNAL EAR 

Stock Vaccines .—Though difficult to explain, it is a fact abundantly 
established by experience that the vast majority of cases of fuiuncles of the 
auditory canal are due to a staphylococcus infection. Utilizing this fact and 
the large clinical material of her clinics and wards, the Manhattan Eye 
and Ear Hospital of New York has for several years used for this lesion 
a stock vaccine made in her own laboratory. This is a composite vaccine, 
i. e., made from various staphylococcus strains derived from pus taken from 
various patients suffering from this particular lesion. There is no question 
that this particular stock vaccine has great value in establishing an im¬ 
munity against recurrence of this distressing lesion. For the rationale of this 
treatment the reader is referred to the short chapter on serum therapy. 

Note —Of recent years the writer has come to regard furunculosis of the meatus 
as a hospital condition. A few days of absolute rest in bed and the better general and 
local care which hospital control makes possible undoubtedly help to a quick and pei- 
manent recovery. 

Acute Diffuse External Otitis—This, according to my experience, is 
a comparatively rare condition. It exists whenever, in the absence of 
determinable foci of infection, the four walls of the canal are in a state of 
acute inflammation. It differs, therefore, from the occasional diffuse 
inflammation of furunculosis in the absence of the localized points of 
infection, single or multiple, which characterize the latter. Another dif¬ 
ference between this and the circumscribed form of external otitis (furun¬ 
culosis) is the frequency with which the whole canal is involved. That is 
to say, furunculosis of the meatus is almost invariably confined to the 
fibrocartilaginous portion, whereas in acute diffuse external otitis the canal 
in its entire length is usually more or less inflamed. 

Causes.— Acute diffuse external otitis may occur as an accompani¬ 
ment of chronic purulent otitis media, in which the discharge from the 
middle ear, being allowed to remain in the meatus, gives rise (1) to mac¬ 
eration and exfoliation of the cutaneous lining, and (2) acts as a direct 
irritant of the exposed subcutaneous surfaces. A more characteristic form 
of acute diffuse external otitis is seen as a result of direct violence, as not 
infrequently occurs in cases in which a physician with more zeal than skill 
has attempted with instruments to remove a foreign body from the meatus. 

Symptoms. —The symptoms are very similar to those observed with 
furunculosis of the meatus,— i.e., pain, sometimes very severe, increased 
by extensive movements of the jaw (yawning) and by any manipulations of 
the auricle which are communicated to the fibrocartilaginous meatus. 
Pressure upon the tragus always causes severe pain. Inspection by re¬ 
flected light shows the calibre of the meatus to be greatly reduced by the 
diffuse swelling of its walls. 

Treatment .—Since the treatment up to a certain point is the same as 
that outlined for furunculosis of the canal, repetition of details are not 
called for. Wet dressings by means of gauze and antiseptic solutions as 
advocated for acute diffuse external otitis, give satisfactory results in a 
large majority of cases. 



Fig. 89.—Hyphomycetes, moulds: A, aspergillus nidulans; B, verticillium Graphii. (After 

Siebenmann.) 











OTOMYCOSIS 


117 


In a quite small percentage of cases, the inflammatory process will 
apparently yield to no treatment short of surgical intervention, which may 
be summed up in a few words: 

(1) Thorough cleansing of the canal, after the method described in 
the treatment of furunculosis. 

(2) One, sometimes two, longitudinal incisions, by means of the furuncle 
knife, through what may appear to be the more acutely inflamed wall or 
walls of the canal. 

(3) Rather prolonged irrigation with a hot solution of boric acid, or 
carbolic acid, 1 in 200. The heat thus applied favors free bleeding, thereby 
relieving tension and tending further to cleanse the parts of bacteria. 

(4) Careful drying of the canal, followed by the introduction of a 
wick of sterile gauze, or of gauze which has been impregnated with Dobell’s 
solution, a solution of boric acid, or^a sterile normal salt solution. The 
dressing should be changed daily, the canal each time being thoroughly 
cleansed. As soon as the inflammation is apparently controlled, better 
results are obtained by a dry dressing, the outer cartilaginous canal being 
firmly packed with a sterile gauze wick. Pressure by this means should be 
continued two or three days after the symptoms and inflammatory signs 
have disappeared. 

Otomycosis.—This term is used to describe the condition in which 
some form of mould has found lodgement, and conditions favorable for 
its development, in the external auditory canal. It may be confined to the 
walls of the bony meatus, or may spread thickly over the drum membrane. 
The fungus may simply inhabit the meatus without causing any morbid 
changes in the tissues upon which it grows, in which case it gives rise to no 
symptoms whatever; and this is the condition found in over one-third of 
all cases (Bezold). In other cases the hyphomycetes may invade the 
tissues, the mycelia perforating the lining membrane of the bony canal 
and the skin covering the drum membrane, and giving rise to an acute 
inflammatory process. 

Etiology.— Beyond the fact that the germ requires warmth and 
moisture for its growth, but little is definitely known as to the cause of its 
frequent occurrence in the ear. Oils and fatty matter form a suitable nidus 
for its development, and Bezold obtained in seventy-five per cent, of all 
cases examined by him a definite history of the patient s having instilled 
medicaments containing oil or glycerin into the ear. 

Many different forms of mould have been demonstrated in specimens 
taken from the ear. Among them may be mentioned the Aspergillus uiger, 
Aspergillus flavus, Aspergillus nidulans, and the T ertidllium graphii .. 

Symptoms. —As before stated, the fungus may remain long in the 
meatus and produce absolutely no symptoms. As soon, however, as the 
mycelia invade the living tissues— d.e., the skin covering the drum mem¬ 
brane or walls of the bony meatus—inflammatory changes aie induced 
and the patient experiences more or less discomfort. The symptoms vary 
from an intense itching and sense of irritation to moderate somethin s 


118 


DISEASES OF THE EXTERNAL EAR 


rather severe—-pain. The hearing may be impaired in cases in which the • 
canal is more or less occluded. 

Inspection by reflected light reveals a different picture according to the 
form of hyphomycetes present and the stage of their development. The 
drum membrane and the walls of the bony meatus may be covered with 
an adherent growth, the color of which may vary from very dark gray or 
black (.Aspergillus niger) to brownish yellow (A. flavus ); or it may be dark 
green in color (Verticillium graphii). Should inflammatory changes have 
taken place, the epithelium covering the drum membrane and canal walls 
may be thickened or exfoliated, or its removal may leave a led and inflamed 
surface. 

Treatment. —Salicylic acid seems to retard or check the growth of 
the various moulds finding lodgement in the ear. The first step in the 
treatment is thorough mechanical cleansing of the parts. The mould 
should first be removed by means of cotton-wound applicators, and the 
canal walls and surface of the drum membrane then carefully scrubbed 
with 95 per cent, alcohol. As a further precaution the ear may be irri¬ 
gated with a 1 per cent, solution of carbolic acid. Lastly the canal is 
filled with a 2 per cent, solution of salicylic acid in alcohol, which is allowed 
to remain in the ear five minutes or more. The patient is given a prescrip¬ 
tion for this solution (i.e., 2 per cent, alcoholic solution of salicylic acid) 
with which he is directed to fill the canal night and morning, allowing it 
to remain from three to five minutes. This treatment usually controls the 
affection fairly promptly, but the patient should be seen occasionally 
during several weeks as a precautionary measure against recurrence. 

When otomycosis occurs in an ear in which the drum membrane is 
perforated, the same line of treatment is usually effective. But since 
the tympanic recesses are not so easily reached, recovery is apt to be 
less rapid. 

Croupous External Otitis (Otitis Externa Crouposa). —This is ad¬ 
mittedly a rare condition. It may be defined as a diffuse inflammation of 
the inner, or tympanic, third of the meatus, in which this part of the canal 
and the surface of the drum membrane are covered by a fibrinous exudate. 
The membrane is repeatedly thrown off in the form of casts of the canal 
and drum-head. A new membrane soon forms. This cycle of exfoliation 
and re-formation may be repeated many times. The condition is some¬ 
what anomalous in providing the only instance of a coagulated fibrinous 
membrane forming upon tissues not covered by mucous membrane. 

Etiology. —Of this but little is definitely known. There are a few 
facts, however, which seem to me somewhat suggestive. It is known, for 
example, that the condition occasionally complicates furunculosis of the 
canal; that in the past it has occurred with comparative frequency in 
certain epidemics of influenza (a disease known frequently to cause blebs 
or bullae of the canal); and that it may be engrafted upon the simple form 
of acute diffuse external otitis. It is possible that the development of the 
lesion requires some form of preexisting acute inflammation plus the action 


FOREIGN BODIES IN THE MEATUS 


119 


of some germ which has not yet been isolated. This theory may help to 
explain its gradual disappearance among the affections treated in aural 
clinics. That is to say, the disease during the past two decades has be¬ 
come exceedingly rare, a fact possibly due to the more general and efficient 
use of antiseptics within that period. 

In a few instances the staphylococcus pyocyaneus and the streptococ¬ 
cus pyogenes have been found in the secretion or casts, but not with suf¬ 
ficient frequency to connect them as specific factors in the causation of 
the disease. 

The symptoms are those common to acute inflammations of the canal, 
—viz., pain in the ear, often very severe,—increasing in severity during 
the formation of new membrane and subsiding as the membrane is dis¬ 
lodged. The hearing is naturally interfered with, and varies in accordance 
with the degree of occlusion of the canal. The course of the disease, 
though often protracted, usually ends in recovery. 

The treatment may be summed up in the word cleanliness. During 
the acute stage frequent irrigation with boric acid solution will help to 
hasten the formation and exfoliation of the membrane. During the periods 
between exfoliation and re-formation of membrane, dry treatment with 
insufflation of boric acid powder is said to give best results. 

OBSTRUCTIVE CONDITIONS OF THE EXTERNAL AUDITORY MEATUS. 

Foreign Bodies in the Meatus.—-There is hardly a limit to the vari¬ 
ety of foreign substances which may be introduced, either intentionally 
or by accident, into the external auditory canal. This is the experience of 
every aurist in hospital practice. Children furnish by far the greater 
number of patients. The writer personally has removed flies, bugs, glass 
beads, imitation diamonds, seeds and small fruit kernels, a bullet, a piece 
of chalk, and a piece of pencil lead. 

In regard to the influence of a small foreign substance in the auditory 
canal, and the supposedly urgent need of its prompt removal, two facts 
should be impressed upon laymen and physicians alike,—viz., (1) that a 
small foreign body may remain in the canal for a long time, or even indefi¬ 
nitely, without injury to the ear and without even causing disturbance of 
function; and (2) that unskilful attempts at removal have frequently 
destroyed the usefulness of the organ, and have been the direct cause of 
not a few deaths. 

Removal of a Foreign Body by Means of the Syringe. —Fortu¬ 
nately, the great majority of foreign bodies finding their way into the 
auditory canal can be removed without injury to the ear by means of the 
syringe. This statement applies to practically all smooth substances 
small enough to enter the bony meatus without having to overcome resist¬ 
ance at the isthmus, and to all smooth bodies remaining in the membrano- 
cartilaginous meatus which are not large enough completely to fill its 
lumen. The fountain syringe is not suitable for this purpose, a syringe 
with which the current force can be regulated by hand pressure being 


120 


DISEASES OF THE EXTERNAL EAR 


infinitely more effective. Fig. 90 shows a metal syringe which can be 
sterilized by boiling and which answers this purpose admirably. 

Before using the syringe the ear should be examined by reflected light 
to determine as nearly as possible the size, shape, and position of the sub¬ 
stance to be removed. If small enough to be freely movable in the canal, 
a few injections of warm boric acid solution, the stream being directed a 
little upward and backward along the posterosuperior canal wall, will 
quickly expel it. When the foreign body has not passed beyond the isth¬ 
mus and is so shaped and situated as to leave a demonstrable space be¬ 
tween it and one wall only of the canal, the stream of water should be 
directed against this open space. In such a case, as soon as the water has 
filled the space between the foreign substance and the drum membrane, 
the principles of hydraulic pressure are brought into play, and the intruder 
is thrown out by the force of the increasing volume of water behind it. 
Were the stream not so directed, it might result in forcing the substance 



into the depths of the bony meatus where its expulsion might be less simple. 
When a foreign body appears completely to fill the lumen of the mem- 
brano-cartilaginous canal, it is clear that irrigation will not dislodge it 
and may carry it further into the canal, unless the stream can be made to 
enter the space between the intruder and the drum membrane. When 
irrigation is employed in such a case, the auricle should be drawn out¬ 
ward and backward, and a rather forcible stream directed inward and a 
little upward and backward along the posterosuperior canal wall. Fol¬ 
lowing this method, the water in most cases reaches the fundus of the 
canal, and the substance is brought away with the return current. 

Insects .—When insects—• e.g ., bugs—are seen crawling within the canal 
or upon the drum membrane, it is well before syringing to fill the meatus 
with olive oil. This dislodges them from their point of attachment and 
facilitates their expulsion. 

Seeds, Peas, etc., within the Canal .—Much has been said of the danger in 
using the syringe of causing'such substances to swell and tightly occlude 
the canal. The question to be considered in such cases is whether the 
pea or seed has already become swollen, or is so large as to render its 








FOREIGN BODIES IN THE MEATUS 


121 


removal by irrigation doubtful; for in case of failure, the moisture left in 
the canal will be likely to render subsequent efforts at removal more diffi¬ 
cult. When, however, the seed or pea is small and movable in the canal, 
there can be no possible danger in the use of the syringe. 

While syringing does not act quite so effectively upon a substance in 
the depths of the bony meatus, there are in the author’s opinion exceed¬ 
ingly few cases in which a foreign body lying free in any portion of the 
canal cannot by this method be removed without injury to the parts. 

Cases Requiring the Use of Instruments. —While the syringe is 
effective in the vast majority of cases, conditions occasionally present 
themselves in which one may be obliged to resort to the use of instru¬ 
ments. In this category may be included the following: 

1. Peas, seeds, etc., of such size, or so enlarged by the effect of heat 
and moisture, as to be no longer freely movable in the canal. 



Fig. 91. 


a 


.^ - * 5 

Fig. 92. 


1 



2. Solid substances which have become so firmly wedged in the canal 
(e.g., at the isthmus or in the depths of the bony meatus) as to require 
mechanical dislodgement. 

3. Solid bodies of irregular or angular shape, pressure of which is 
causing inflammatory swelling of the membrano-cartilaginous meatus. A 
deft use of instruments is often the only means of relieving this condition. 

4. Solid substances which have been forced into the bony meatus, 
and are yet too large to repass the isthmus on the way out except in i esponse 
to an equal amount of force. Children occasionally furnish such instances. 

Choice and Use of Instruments— In the author’s opinion the safest 
instruments for removing solid substances from the eai aie those typified 
in the accompanying illustrations. 

The hook (Fig. 91) should present a terminal rectangular bend about 3 
mm. in length, the extremity of which is rounded or dull. In using it the 
hook, or terminal bend, lying flat against the canal wall, is cairied past the 
intruding substance. The handle, or shaft, is then rotated so that the hook 
squarely engages the foreign body, which can usually be easily withdrawn. 
This in my experience is a very practical little instrument which can be 
successfully employed in a majority of cases. 
























122 


DISEASES OF THE EXTERNAL EAR 


The dull ring curette (Fig. 92) can be used safely in only one way: it 
should be introduced either above or behind the body to be removed, i.e., 
between it and the roof or the posterior canal wall. The body is then 
crowded downward or forward against the floor or anterior wall, and thus 
pushed outward toward the orifice of the canal. Pressure with the ring 
curette from below upward is always dangerous, for the reason that it may 
force the substance backward upon, and even through, the drum membrane. 

The author’s adjustable ring curette (Fig. 93) is practically a dull ring 
curette in which, by sliding forward a movable rod, the ring can be made to 
assume a position at right angles to the shaft. Its application is obvious. 
The ring in the straight position is carried beyond the substance to be re¬ 
moved, and then changed into the rectangular position, in which it cannot 
fail to engage the intruder. 

The writer has purposely not mentioned any form of forceps, because 
he believes that a forceps should never be used for removing a solid body 
from the auditory canal. The two main objections to its use may be 
stated as follows: 

1. In removing a foreign body it is particularly important to avoid 
any injury to the canal. With care it is almost always possible to pass a 
small instrument between the intruding body and one wall of the meatus 
without injiuy to the latter. With the forceps, however, one has in effect 
simultaneously to pass two instruments— i.e., the two forceps blades 
—'between opposite sides of the foreign body and the corresponding canal 
walls. Unless the body is so small as to be obviously removable by the 
syringe, the danger of traumatism is doubled. Bleeding in case of failure 
renders further effort more difficult. 

2. The chief objection to the forceps, however, is the danger of push¬ 
ing the offending substance further into the canal. Not infrequently a 
solid, smooth substance, which seems easily and safely within the grasp of 
the forceps, slips from its blades and is driven further toward the drum 
membrane. Successive attempts may result not only in further displace¬ 
ment, but often in extensive laceration of the canal. The writer has 
known more than one case in which the drum membrane has been practi¬ 
cally destroyed by this manoeuvre, the foreign body being finally pushed 
into the tympanic cavity. Every experienced aurist has met with such cases. 

Surgical Removal of a Foreign Body from the Meatus. —This is advisable 
whenever it becomes evident that the simpler methods above described 
cannot be employed successfully or without endangering the integrity of 
the organ. The conditions calling for operative intervention fall chiefly 
under two heads,—viz.: 

(a) Inflammatory swelling of the canal so occluding its lumen that small 
instruments cannot be manipulated within the meatus without danger of 
injury to the deeper parts. Under such conditions the attempt to remove 
a foreign body through the meatus might result in irreparable injury to 
the ear. 


REMOVAL OF CERUMEN FROM THE MEATUS 


123 


(b) The aurist has occasionally to deal with cases in which ill-advised 
or unskilful attempts at removal have resulted in such traumatism of the 
canal walls that the exact size and position of the foreign body and the 
condition of the tympanic structures cannot be determined. Under 
such conditions further attempts at removal through the canal are apt 
to result in further injury. 

It should be accepted as an axiom in practical otology that no instru¬ 
ment should be introduced into the meatus except under inspection by 
reflected light, and under conditions permitting one to know positively 
its exact position after it has entered the bony canal. Obviously, when 
the canal is swollen or bleeding, or its walls torn and lacerated, the use of 
instruments cannot be controlled by the recognition of familiar land¬ 
marks. Under such circumstances the attempt to carry an instrument 
beyond a foreign substance may result in serious injury to important 
tympanic structures, or even in dislocation of the stapes from the oval 
window. Bezold is authority for the statement that such accidents have 
been responsible for many deaths. 

Students of otology will do well to bear in mind and adhere strictly to 
the following rule: Whenever the membrano-cartilaginous canal is acutely 
inflamed, no attempt should be made to remove a foreign body even from the 
older, or membranous, portion of the meatus, without having the patient under 
the influence of a general anaesthetic. With the patient anaesthetized, it is 
usually possible, even in the presence of moderate inflammation, to remove 
through the canal a foreign substance which has not passed into the 
bony meatus. 

The steps of the operation for removing a foreign body from the depths 
of the bony meatus are as follows: A curvilinear incision, following the 
curve of the auricular attachment, is made over the mastoid process. This 
incision passes through all the soft tissues, including the periosteum, down 
to the bone. The periosteum is carefully elevated anteriorly, and the lin¬ 
ing membrane of the bony canal separated from its walls by means of a 
small curved elevator. Under traction the membranous canal is usually 
torn from its attachment to the annulus tympanicus and the drum mem¬ 
brane, and the auricle is folded forward upon the face, drawing with it the 
membranous canal out of the bony meatus. It is now an easy matter to 
remove the foreign body with forceps or other instrument, unless it has 
been forced through the drum membrane by previous manipulation, and 
lies hidden within one of the recesses of the tympanic cavity. After the 
intruder has been removed, the parts, having been re-sterilized, are re¬ 
placed in position, and the posterior wound sutured. The membranous 
lining of the bony canal is held in place by a light packing of sterile gauze. 
If asepsis has been carefully observed, the wound resulting from this 
operation usually heals promptly. 

In certain cases it will be found that, as a result of previous ill-advised 
attempts at its removal, the foreign body has been forced through the 
drum membrane, and therefore lies within the tympanic cavity proper. 


124 


DISEASES OF THE EXTERNAL EAR 


Under such conditions it may be necessary to enlarge the opening in the 
drum membrane or even to remove it in order to locate the object which 
has been the cause of so much needless injury. In two cases operated upon 
by the writer, the drum membrane had been torn and lacerated beyond 
any hope of repair, before the patient came under his care. 

Removal of Cerumen from the Meatus.—The secretion of cerumen, 
or “ear-wax,” is confined to the area of distribution of the ceruminous 
glands in the outer part of the membrano-cartilaginous meatus. In amount 
it varies in different individuals from a very thin layer lining the outer end 
of the canal to large masses completely occluding its lumen. In a certain 
proportion of cases there is practical absence of cerumen so far as the eye 
can detect. These differences may occur in ears which are otherwise 
perfectly normal. Ordinarily the cerumen is confined to the outer, or 
membranous, portion of the canal. In some cases, however, in which there 
is no automatic elimination or extrusion of the cerumen formed, the last 
to be secreted pushes the previously formed mass further inward toward 
the drum membrane, and this process, repeating itself, finally completely 
fills the meatus. 

When present in the meatus in masses large enough to disturb or 
endanger the auditory function, cerumen becomes practically a foreign 
body, which should be removed. The method of removing it calls for 
but brief notice here, since it is effected by practically the same measures 
as have been described for removing foreign substances finding their way 
into the ear. In the vast majority of cases, even large masses of cerumen 
may be removed easily and without injury to the canal by means of the 
syringe. As occasional exceptions to this rule may be mentioned the 
following conditions: 

(a) The presence of large masses of tightly impacted cerumen com¬ 
pletely closing the membrano-cartilaginous canal. In such a case the 
stream of water from the syringe may play upon the obstructing mass, 
exerting no influence upon its position. If we can insinuate a dull ring 
curette or other small instrument between the roof of the canal and the 
cerumen, we may by crushing the latter downward be able to create a 
passage by which the irrigation fluid may reach the fundus of the canal. 
By directing the stream along this pathway, the cerumen will in many 
cases be quickly expelled. Should this fail, it may be necessary to intro¬ 
duce a hook, or the angular ring curette, into the space above described 
and remove the cerumen by direct traction. 

(b) A second condition for which the syringe is inadequate is found 
in cases in which the whole canal from the external orifice to the drum 
membrane is filled by a solidly packed mass, probably representing the 
accumulation of years. Such an accumulation is usually composed of 
cerumen intermixed with layers of exfoliated epithelium, finally becom¬ 
ing welded into an exceedingly hard and impervious mass. This condition 
is made known to us first by the inefficacy of the syringe, and second by 
the sense of solidity and resistance which it imparts to the probe or curette. 


EXOSTOSES OF THE OSSEOUS MEATUS 


125 


In this condition I believe that it is not always best to attempt to remove 
the entire mass at one sitting. If we can succeed in passing a dull ring- 
curette for a short distance between the canal roof and the obstructing body, 
we may be able to force the ring down into it, and thus by traction with¬ 
draw the entire mass, or a portion of it. If only a part of the mass comes 
away, we may proceed in like manner to remove piecemeal so much of 
what remains as can be dislodged without injury to the canal. As soon, 
however, as we find ourselves in danger of injuring the canal walls, it is 
better to desist. We now direct the patient to fill the meatus night and 
morning with a solution of bicarbonate of soda (gr. xx ad g i), and to irri¬ 
gate the ear once daily with a warm solution of boric acid (5 j to the pint). 
If in two days this has not resulted in clearing the canal, we shall in most 
cases find the mass so much softened that we shall have little difficulty in 
removing it. 

In some cases the use of the syringe leaves the drum membrane red 
and inflamed in appearance, a condition which usually subsides rapidly. 

Exostoses of the Osseous Meatus; Bony Outgrowths from the 
Walls of the Bony Canal.—Hut little is known of the etiology of these 
growths. According to Bezold, they represent a condition rarely or never 
developed before puberty. They are multiple oftener than single, appear¬ 
ing oftenest on the anterior and posterior walls. When one growth only 
is present, the anterior wall, near the attachment of the drum membrane, 
is the most common site. As seen by reflected light, they appear as small, 
rounded protuberances, covered by normal skin, into the lumen of the 
canal. Palpation with a silver probe shows them to be hard and rather 
insensitive to pressure. 

It is rare for these growths to occlude the canal completely, and the 
hearing is not usually noticeably impaired. Only in the case of acute 
middle-ear suppuration do exostoses of the canal cause anxiety, and then 
only if they are sufficiently large to interfere with drainage or the proper 
management of the tympanic lesion. 

Treatment. —Usually none. Unless occluding the canal or unfavor¬ 
ably influencing the course of a middle-ear lesion, removal is not indicated. 
Should conditions arise rendering removal imperative the method of 
accomplishing this depends upon the character of the growth. If it is 
attached to the bony canal wall by a slender pedicle, it may be an easy 
matter to detach it by a single light tap upon a narrow chisel, the edge 
of which is held in firm contact with the canal wall at the point to which 
the pedicle is attached. When, however, the growth is attached by a 
broad base, no attempt should be made to remove it through the membrano- 
cartilaginous meatus. In such a case it is far safer to make a curvilinear 
incision behind the ear and carry the auricle forward upon the face, sepa¬ 
rating and lifting the membrano-cartilaginous meatus out of the bony 
canal. The bony growth may then be removed by means of a small chisel 
or gouge, or it may be practical and safe to introduce a small sharp bone 
curette and remove it from within outward. 


CHAPTER V. 

CAUSES OF ACUTE TYMPANIC DISEASE. 

The conditions which predispose to, or excite, middle-ear inflammation 
may give rise to the mildest type of tympanic congestion or to the severest 
form of suppurative otitis media. That is to say, it is not possible, in the 
light of our present experience and knowledge, to speak dogmatically of 
one group of etiological factors as producing the milder ear lesions and of 
another as responsible for the severer types of tympanic disease. It will, 
therefore, enable us to avoid much useless repetition, and also conduce to 
a clearer and more practical view of the subject, to speak first of the causes 
of acute tympanic inflammation in general. It will then suffice to mention 
with each recognized type of otitis media the causes to which it is most 
often traceable. 

Predisposing Causes.—Of predisposing constitutional conditions but 
little may be said beyond the fact that conditions of lowered vitality 
render the individual more susceptible to suppurative middle-ear lesions 
than are the physically and constitutionally robust. Only in this way can 
be explained the enormous prevalence of suppurative otitis media among 
the ill-nourished and poorly housed children of the poorer class of tenement- 
house dwellers in the large cities. The extent of this predisposition is not 
generally recognized either by the laity or by the medical profession, for 
the reason that, when drainage from the ear has once been established by a 
large perforation in the drum-head, the little patients suffer no pain and 
usually no constitutional symptoms sufficiently pronounced to attract 
attention. Should any physician in large dispensary practice among chil¬ 
dren care to investigate the truth of these statements, he may do so by 
making systematic aural examinations in any large series of cases. Such 
a series of examinations, if the results were carefully noted and the 
number of cases examined were sufficiently large, would not only be in¬ 
structive to him, but might form the basis of a record of considerable value 
alike to otologists and to physicians generally. 

Age. —Children undoubtedly suffer more frequently from acute middle- 
ear disease than adults. This is due in part (a) to the influence of pharyn¬ 
geal adenoids, which are oftener present during childhood than in adult life; 
(b) to the greater susceptibility of children to the acute infectious diseases 
which so often give rise to otitis media; and (c) to certain anatomical dif¬ 
ferences in the Eustachian tubes in infancy and young childhood as com¬ 
pared with the adult type. These differences are described in the chapter 
dealing with the anatomy of the conducting apparatus. 

Nasal Obstruction. — Undoubtedly the most potent predisposing 
cause of tympanic disease is to be found in conditions interfering with 
nasal respiration. Here again, with regard to acute otitis media, children 
126 


ACUTE INFECTIOUS DISEASES 


127 


are the greater sufferers. The presence in the nasopharynx of large 
masses of adenoid tissue, with or without great enlargement of the faucial 
tonsils, constitutes a constant menace to the ears, which can be corrected 
Only by removal of the growth. The important relation of adenoids to 
tympanic disease is made clear by the following facts, which may be veri¬ 
fied by any physician who will take the time and trouble to do so: 

(1) A majority of all cases of acute otitis media in children occur in 
those suffering from adenoids. 

(2) Conversely, examination of any series of children suffering from 
adenoids will show in a majority of cases some pathological condition in 
one or both ears. 

(3) Children with large adenoid growths rarely pass through a severe 
exanthematous attack without aural complication,— i.e., without some 
grade of tympanic inflammation. And, 

(4) Conversely, children without hypertrophy of the pharyngeal and 
faucial tonsils, or in whom adenoids have been successfully removed, 
usually pass through the infectious diseases of childhood without middle- 
ear inflammation. 

Among other lesions interfering with nasal respiration are the following, 
which more commonly give trouble in adult life: Marked deviations to one 
or the other side of the nasal septum; septal ecchondroses or exostoses 
(commonly called spurs); hypertrophic rhinitis. These conditions predis¬ 
pose primarily to catarrh of the nasopharynx and membrano-cartilaginous 
portion of the Eustachian tube, and secondarily to middle-ear inflammation. 

Exciting Causes.— Acute Rhinitis. —Acute middle-ear inflammation 
occurs very frequently as an accompaniment or immediate sequela of 
acute coryza, the common “cold in the head A The author has made a 
habit of questioning his dispensary patients, as well as those in private 
practice, as to conditions or causes to which an existing acute otitis might 
be traced. That it followed “a severe cold” is a very frequent answer, 
but even more numerous are the cases in which absolutely no data upon 
which to base a theory as to its causation can be elicited from the patient. 
These cases can hardly be regarded as idiopathic, and are probably to be 
explained as having followed a mild coryza, or nasopharyngeal catarrh, 
which has escaped the patient’s memory. The writer believes that more 
cases of acute otitis media residt from a simple nasopharyngitis, acting upon 
an individual in whom strongly predisposing conditions exist, than can he 
traced to all other exciting causes combined. 

Acute Infectious Diseases. —Just what percentage of cases of the 
acute exanthemata give rise to acute aural disease has not been deter¬ 
mined. The author, as aural surgeon to the Willard Parker Hospital 
(New York city hospital for infectious diseases), has had some oppor¬ 
tunity of observing the aural complications of certain inlections notably 
in scarlet fever and diphtheria. Taking these diseases lor purposes ol 
comparison, he would say that at least 10 per cent, of all case ol scarlatina 
and 5 per cent, of all cases of diphtheria develop some form of acute 


128 


CAUSES OF ACUTE TYMPANIC DISEASE 


tympanic disease. Were the ears of all children suffering from these 
diseases examined daily, there is little doubt that a larger percentage of 
cases of acute tympanic disease would be diagnosticated than is repre¬ 
sented by those usually attracting the physician’s attention. Measles gives 
rise to acute suppurative otitis media, often of severe type, and in a percent¬ 
age of cases probably falling little short of that associated with scarlet fever. 

As to the comparative average severity of the aural lesions complicat¬ 
ing the various exanthemata, it may be said that the purulent otitis media 
associated with measles is of severe average type, and that the percentage 
of cases developing suppurative mastoiditis is particularly large. The 
tympanic inflammation complicating scarlatina comes next to that associ¬ 
ated with measles in the frequency with which the mastoid cells become 
infected. Another very serious and characteristic feature of scarlatinal 
otitis media is the astonishing rapidity with which the drum membrane 
may be actually destroyed. The writer has seen cases in which the pos¬ 
terior segment of a perfectly normal drum membrane has undergone almost 
complete disintegration within a few days of the onset of a scarlatinal otitis 
media. The destruction of the drum-head is in some cases so rapid and 
extensive as to render it impossible, after the systemic disease has run its 
course, for the tympanic defect to be repaired and the middle ear to regain 
its normal condition. This explains the very large percentage of clinic 
patients, suffering from chronic suppurative otitis media, who trace their 
aural lesions back to an attack of scarlet fever. 

As compared with measles and scarlet fever, the aural complications 
of diphtheria are both infrequent and mild. There is greater danger of 
extensive destruction of the drum-head than of rapid and serious involve¬ 
ment of the mastoid cells. As with other infectious diseases, however, 
different epidemics vary greatly in the type of aural lesions produced. 
While in New York during the past three or four years the aural compli¬ 
cations of diphtheria have been of comparatively mild type, the author 
recalls certain seasons in which the disease gave rise to many instances of 
severe tympanic and mastoid suppuration. Among the further results 
of such lesions he recalls one fatal case of brain abscess, several cases of 
purulent leptomeningitis, and a still greater number of cases of infective 
sigmoid sinus thrombosis. 

Grippe, or influenza, is a frequent cause of more or less severe purulent 
otitis media, which in certain epidemics shows a marked tendency to rapid 
involvement of the mastoid cells. 

Typhoid fever is a comparatively rare factor in the causation of acute 
tympanic disease. The aural lesions are in no way distinctive, or different 
from those occasionally accompanying other wasting diseases. The end 
of the third week and throughout the fourth week are said to cover the 
period during which aural lesions are most likely to develop. 

Parotitis, or mumps, happily seldom causes tympanic suppuration. 
When the ears do become infected as a result of this disease, the labyrinth 
as well as the tympanum is not infrequently involved. This form of 


EXCITING CAUSES OF TYMPANIC DISEASE 


129 


panotitis may follow the usual course of a suppurative labyrinthitis; or 
the vestibular symptoms may rapidly subside, leaving in their wake ex¬ 
treme or even total deafness. It is one of the unhappy consequences of 
this lesion that the deafness, if pronounced, is apt to be permanent. Par¬ 
tial restoration of the cochlear function is said in certain cases to have 
been observed. Usually no improvement occurs. 

External Causes. —Most of these are conditions which give rise to 
nasal or nasopharyngeal congestion. Thus, sudden or prolonged exposure 
to cold or getting the feet wet may cause grippe, pharyngitis, or only an 
acute rhinitis, any of which conditions may lead to acute tympanic disease. 
Inhalation of irritating vapors may act in much the same way. Thus, the 
use of fast automobiles by exposing the individual to sudden chilling of 
the surface or to the inhalation of heavily dust-laden air, has been respon¬ 
sible for some cases of acute otitis media. 

The Nasal Douche .—The nasal douche, so frequently advised by some 
rhinologists and in some clinics, is doubtless absolutely necessary in certain 
cases of ozsena or of advanced atrophic rhinitis. It is also, however, a not 
infrequent cause of acute otitis media. Cases of aural disease originating 
in this way are known to every aurist. The author knows of at least one 
case in which the use of the nasal douche was directly followed by acute 
suppurative inflammation with mastoid involvement of both ears. Opera¬ 
tion upon both mastoids revealed pus and extensive caries throughout 
both processes. In this case the patient said that, on using the douche for 
the first time, he choked slightly and “felt the fluid go to the ears.” It 
is certainly safer, so far as the ears are concerned, to prescribe a nasal 
spray (atomizer) in place of the douche in all cases in which the nasal 
douche is not absolutely necessary. 

Swimming or diving in cold water is another prolific cause of acute 
aural disease, which brings many recruits to the aurist and aural clinic 
with each return of the swimming season. It is probable that this cause 
acts in two ways—viz. (1) through water taken into the mouth, some of 
which is propelled through the Eustachian tubes to the middle ear; and 
(2) by the impact of the water against the membrana tympani. It is to 
be guarded against, therefore, (a) by stopping the ears by means of a wad 
of moistened absorbent cotton, and (b) by care to avoid choking or violent 
efforts to expel water taken into the mouth or nose while under water. 

In a general way the above conditions may be said to constitute the 
chief etiological factors in the various types of acute middle-ear disease. 
Their importance in otology is obvious. The aurist who relieves the symp¬ 
toms of an acute attack, but takes no thought of precautions to prevent 
recurrences or the development of the insidious chronic processes which 
may follow, hardly fulfils his whole duty toward the patient. And this 
obligation can be met only by careful consideration of the underlying 
causes in each case of tympanic disease. If we consider what might be 
accomplished in the way of preventing aural disease, the responsibility of 
the general practitioner is quite as great. In no branch of preventive medi- 
9 


130 


CAUSES OF ACUTE TYMPANIC DISEASE 


cine are the possibilities greater. If it were more fully realized that the 
presence of adenoids, when sufficiently large to interfere in any degree 
with nasal respiration, almost invariably causes tympanic congestion; 
that their removal minimizes the danger of tympanic infection; that the 
infectious diseases of childhood give rise to suppurative otitis media more 
frequently than acute articular rheumatism gives rise to endocarditis, it is 
clear that the prevalence of aural disease among people of all ages might be 
very appreciably reduced. 

Occupation and Habits as Causes of Aural Disease—That certain 
occupations and habits may predispose to, or excite, aural disease, there 
is no room for doubt. Recognition of this fact and observation of certain 
forms of aural disorder thus induced have led to their being spoken of as 
“occupational diseases.” This is an unscientific term which, however, has 
served a useful purpose in directing attention to certain vicious influences 
which should as far as possible be guarded against. Certain occupations 
and certain habits predispose to, or cause, certain forms of aural disease, 
but there is no evidence that the diseases in question differ in pathology 
or symptomatology from the corresponding disorders due to other causes. 

Among the habits or occupations which occasionally cause aural disease 
or disorder may be mentioned the following: (1) The habitual or frequent 
use of certain drugs, — e.g., tobacco, alcohol, the coal-tar products 
(phenacetine, etc.). (2) Occupations in which the individual habitually 
breathes heavily dust-laden air,— e.g., railroad engineers, firemen, con¬ 
ductors, and others employed upon fast-moving trains; chauffeurs; street- 
sweepers, etc., etc. (3) Occupations subjecting the individual to the 
constant or frequently recurring influence of loud noises,— e.g., black¬ 
smiths, boiler-makers, naval and field officers and men subjected to the 
reports of heavy ordnance, workers in factories who are subjected to a 
constant roar of machinery. (4) Occupations requiring sudden or prolonged 
changes of air pressure, (a) upon the drum membrane, as in the case of 
caisson workers, or (b) within the tympanum,— e.g., cornet-players and per¬ 
formers upon wind-instruments generally. (5) Workers in substances con¬ 
taining certain systemic poisons,— e.g., lead, arsenic, phosphorus, aniline, etc. 

In consideration of the many who, though subjected to one or other of 
the above influences, escape wholly any untoward result, one is forced to 
assume that individual idiosyncrasy or especial vulnerability to certain 
influences, or substantial powers of resistance to the same, must consti¬ 
tute in some cases a determining factor. It is also necessary to assume that 
in many cases the causal factor may act in two ways,— i.e., either upon 
the sound-conducting mechanism or upon the labyrinth or auditory nerve. 

As to the varying susceptibility of different individuals to certain 
influences, tobacco and alcohol furnish notable examples. Thus, one man 
may be able to smoke habitually large numbers of cigars daily and to 
drink wine, beer, or whiskey in considerable amount without any determ¬ 
inable injurious effect upon his ears, while another suffers regularly from 
any excessive indulgence in either. 


OCCUPATIONAL CAUSES 


131 


Tobacco in susceptible subjects may affect the ears injuriously in two 
ways,— i.e., (a) by inducing venous congestion or catarrh of the tubal 
mucosa, this giving rise to alterations of intratympanic pressure and ten¬ 
sion; or (b) more rarely, may induce a slow and insidious form of auditory- 
nerve deafness. A colleague of the writer who has been an habitual though 
moderate smoker of cigars has been obliged to give up smoking on account 
of the aural symptoms induced. He states that whenever he is tempted 
to smoke, even in moderation, he regularly experiences tinnitus aurium 
and a sense of fulness and occlusion of the ears, which as regularly disap¬ 
pear after a few days of abstention from tobacco. In such a case the aural 
symptoms are clearly due to a mechanical interference with the functional 
activity of the Eustachian tubes. 

As to the influence of alcohol upon the ears, while it is generally ad¬ 
mitted that alcoholic excesses may be injurious to the auditory as to other 
cranial nerves, a search of the literature yields little that bears directly on 
the subject. The most authentic and apparently typical cases reported are 
those of two university students observed by the late Professor Bezold. 
These patients experienced sudden, very marked loss of hearing. Careful 
functional tests demonstrated a type of deafness characteristic of labyrin¬ 
thine rather than of tympanic disease. Interrogation elicited the fact that 
both patients had for some months been in the habit of consuming enor¬ 
mous quantities of beer. All indulgence in alcoholic drinks was stopped, fol¬ 
lowing which there was a gradual but complete restoration of hearing power.. 

Characteristic alcoholic deafness is probably in most cases dependent 
upon a neuritis of the auditory nerve, which, if the cause is not removed,, 
leads to degenerative changes and permanent deafness. 

Occupations subjecting their followers to more or less constant breath¬ 
ing of dust-laden air— e.g., railway employes, chauffeurs, workers in dust- 
filled factories, etc.—are naturally productive of nasopharyngeal and 
tubal catarrh and the type of deafness characteristic of the tympanic 
changes secondary to such lesions. 

Occupations in the pursuit of which the individual is subjected to the 
ear-strain or shock of constant or very loud noises, give rise to two types 
of deafness, both of which are due to labyrinthine injury or disturbance. 
Blacksmiths, machine-workers, workers in factories in which a constant 
whirr of machinery is heard, suffer sooner or later a diminution of hearing 
which is of the type characteristic of a labyrinthine or nerve lesion. In the 
case of continuous or frequently recurring noises, it is supposed that the 
more or less prolonged irritation of the auditory nerve filaments leads in 
time to degenerative nerve changes of which the loss of auditory acuteness 
is a logical manifestation. The auditory nerve changes in these cases are 
probably in some degree analogous to those induced by Siebenmann and 
Wittmaack in their experiments upon animals. It will be remembered 
that these investigators, in experiments separately carried out, subjected 
animals to the continuous sounding of certain musical tones, with the re¬ 
sult that pathologic changes were induced in certain definite structures of 


132 


CAUSES OF ACUTE TYMPANIC DISEASE 


the perceptive mechanism, the site of these changes varying with the 
musical tone employed. Substituting for the prolonged hearing of a single 
musical tone the constant repetition of loud noises irritating to all parts of 
Corti’s organ, it is not surprising that morbid changes leading to impaired 
hearing should result. 

The cases of sudden, and often very profound, deafness following very 
loud explosive sounds— e.g., the report of a cannon, the explosion of a mine, 
etc.—are obviously of quite different origin from those above described, 
these latter being due most probably to hemorrhage into the labyrinth or 
to sudden paralysis of the eighth nerve. That the symptoms, in some 
cases at least, are the result of changes primarily involving the auditory 
nerve filaments within the labyrinth is evidenced by the fact that the 
vestibular branch is also frequently disturbed. 

Occupations requiring sudden or prolonged changes of air pressure 
upon the drum membrane or within the tympanum, most frequently 
give rise to morbid changes confined to the tympanum. This is usually 
the case in occupations calling for frequent increase of intratympanic 
pressure,— e.g., cornet-players, glass-blowers, etc. The aural lesions to 
which caisson-workers are subject are also in a majority of cases confined 
to the tympanum, but occasionally involve the labyrinth. 

In regard to the aural disorders of caisson workers, a word should be 
said as to the two very distinct lesions which this occupation may inflict 
upon its followers. 

1. The first, and fortunately the commonest, is due to the great increase 
of atmospheric pressure to which the tympanic mucosa is subjected. 
Unless the tubes are absolutely patent the drum membranes are forced 
inward. In either case the mucous membrane lining the tympanic walls 
and drum membrane is subjected to enormous uniform increase of pres¬ 
sure, which when he leaves the caisson is as suddenly relieved. These 
sudden changes induce in some cases a most aggravated form of tympanic 
venous congestion, characterized in some cases by ecchymoses into the 
drum membrane, or hemorrhage into the tympanum. The symptoms 
are tympanic in character, alarming to the patient on account of their 
sudden advent, but usually yielding to time and rational treatment. 

2. The second and more serious lesion of the caisson worker is a laby¬ 
rinthine disorder the patholog}^ of which is somewhat obscure. According 
to the theory of those who have made a study of it (Alt, Heller, H. v. 
Schrotter), the disease is the result of sudden alterations in the composi¬ 
tion and density of the blood. As a result of the sudden diminution of 
atmospheric pressure when the individual leaves the caisson, arterial 
pressure is increased to the point of causing labyrinthine hemorrhage. 
Another theory is that the sudden decompression incident to leaving the 
caisson results in the formation within the blood of gas emboli, lodgement 
of which within the labyrinth is the direct cause of the lesion. The symp¬ 
toms are those characteristic of labyrinthine hemorrhage—vertigo, ataxia, 
deafness. In severe cases the deafness is profound and may be permanent. 


CHAPTER VI. 

THE SUBJECTIVE SYMPTOMS OF AURAL DISEASE. 

There are just four symptoms referable to the ear of which a patient 
suffering from any form of aural disease, acute or chronic, may complain,— 
viz.: (1) aural pain, or earache; (2) impaired hearing, or deafness; (3) 
aural discharge; and (4) tinnitus aurium, or the subjective sensation of 
noises in the ear. One or more of these symptoms will be present in any 
aural disorder. Vertigo and ataxia, which are such important symptoms 
of certain disorders of the labyrinth, are purposely omitted from this list, 
which is intended to include only the commoner phenomena which the 
patient himself would recognize as of aural origin. 

Before entering upon a discussion of the more important middle-ear 
lesions, it may be well to consider briefly these subjective phenomena, 
which convey to the patient the knowledge that his ear is diseased. 

Aural Pain.—Earache is present at some stage of practical^ every 
case of acute middle-ear inflammation. It may also be present (though 
comparatively rarely) in certain stages of chronic non-suppurative middle- 
ear disease. It is an invariable accompaniment of acute inflammatory 
disease of the membrano-cartilaginous meatus, and it may occur in very 
severe type as a reflex phenomenon from lesions widely separated from 
the ear. For purposes of differentiation, all of these types will be briefly 
discussed. 

Pain in Acute Otitis Media. —The earache of acute catarrhal or 
purulent otitis media is described as resembling the pain of a severe tooth¬ 
ache,— i.e ., throbbing or drawing in character, subject to exacerbations 
of intensity,—but of greater severity. It is probably one of the most 
unbearable types of physical pain. Its onset is usually sudden. Follow¬ 
ing a few premonitory twinges, the pain quickly attains a degree of inten¬ 
sity which makes sleep impossible. It is not influenced by manipulation 
or movements of the auricle or membrano-cartilaginous meatus. It is due 
either to increased tension through engorgement of the tympanic vessels, 
or to pressure and distention by fluid (serum or pus) collecting within the 
tympanic cavitjL It is, therefore, often of short duration, subsiding quickly 
after spontaneous rupture of the drum membrane. This fact suggests the 
clearest indication for its relief: Free incision of the drum membrane almost 
invariably relieves the pain of acute middle-ear inflammation. 

Pain in Chronic Catarrhal Otitis Media.— Another type of ear 
pain which may puzzle even the experienced aurist is a form of paroxysmal 
earache of moderate grade which is far commoner in chronic catarrhal 
otitis media than is commonly recognized. The patient gives a history of 
more or less frequently recurring attacks of otalgia, which, however, do 
not seem ever to be as severe as the pain accompanying acute t\ mpanic 


134 


SUBJECTIVE SYMPTOMS OF AURAL DISEASE 


disease. The drum membranes may present changes characteristic of 
chronic catarrhal otitis media, but no sign of acute inflammation. In 
the mouth and throat are found no lesions of which the ear pain might be a 
reflex phenomenon. Under such conditions careful testing of the hearing 
will in many cases show the progress of a chronic middle-ear inflammation, 
with the periodic extensions of which the pain is probably associated. 

Pain in Furunculosis of the Meatus. —The earache accompanying 
this lesion presents certain fairly constant characteristics. It is commonly 
gradual in its development, beginning as a sense of soreness about the 
canal, which later changes into a constant, throbbing pain of very severe 
type. It has frequently this pathognomonic characteristic,— i.e., that it is 
increased or intensified by wide movements of the jaw,— e.g., in yawning, 
or even chewing. This practically locates the lesion in the membrano- 
cartilaginous meatus, though the lesion may be either circumscribed or 
diffuse. Naturally the pain is intensified by any manipulation of the pinna 
which moves the cartilaginous meatus. As compared with the earache of 
acute purulent otitis media, the pain of furunculosis of the meatus is more 
gradual in its development and often less quickly relieved. While the 
indication is clearly a free incision through the focus of infection, this does 
not always furnish immediate relief of the pain. 

Reflex Aural Pain. —Patients seeking relief from very severe ear¬ 
ache, in whom physical examination shows the ears to be practically 
normal, are by no means uncommon in otological practice. In such cases 
we must carefully examine the mouth and throat for acute lesions which 
may be the underlying cause. By far the commonest cause of reflex aural 
pain is dental caries. Every aurist has seen such cases,-— i.e., the patient 
suffering acutely from aural pain, the drum membranes being practically 
normal, and one or more teeth of the corresponding side of the jaw being 
carious. The writer recalls the case of an intelligent, but nervous, woman 
who rather indignantly combated the suggestion of dental caries as the 
cause of very severe earache, which, however, was not relieved until a 
necrotic tooth was removed. The only relief in such cases is obtained 
through the dentist. 

Other lesions causing reflex otalgia are severe acute tonsillitis, peri¬ 
tonsillar abscess, malignant disease of the base of the tongue. 

Impairment of Hearing. — Some degree of functional impairment, 
transient or permanent, is probably present in every case of tympanic 
disease. Unfortunately, very slight grades of impairment are commonly 
not recognized by the patient. This is the more unfortunate since the 
onset of chronic non-suppurative otitis media is the stage in which most 
could be done to prevent progress of the lesion and the development of 
disabling deafness later in life. It is important, therefore, that very care¬ 
ful hearing tests should be made in all cases of slight aural disorder. 

In acute middle-ear inflammation the hearing tests are not so important 
during the attack as after it has run its course, when a careful functional 
examination may demonstrate a residual disturbance of hearing which 


AURAL DISCHARGE 


135 


may be easily corrected by appropriate measures promptly applied. 
Neglect at this stage may pave the way for chronic changes resulting in 
marked deafness later in life. 

Aural Discharge.—Discharge from the ear, resulting from tympanic 
disease, always signifies partial or complete destruction of the mem- 
brana tympani,— i.e., a perforation which may vary from a pin-head 
orifice to practical loss of the membrana tensa. It may be scanty or pro¬ 
fuse; serous or purulent, and may be tinged with blood; odorless or ex¬ 
ceedingly offensive. Since the character of the discharge necessarily calls 
for discussion in connection with the various lesions, but little need be 
said here beyond the mention of certain points in which the discharge 
in acute otitis media usually differs from that of chronic middle-ear 
suppuration. 

Discharge in Acute Otitis Media. —Bacteriologically it varies in 
accordance with the character of the infection,— i.e., it may contain any 
of the pus-forming bacteria, or in a purely serous inflammation may be 
mucoserous and sterile. Usually, however, an aural discharge remains 
sterile only a short period after incision or perforation of the drum-head, 
— i.e., it soon becomes infected by germs from without. 

Except when allowed to remain long in the canal, the discharge in 
acute otitis media is usually without odor. Following incision of the drum 
membrane the discharge is often at first very moderate in amount, but 
rapidly increases during the first twenty-four hours thereafter. Following 
this initial period, the discharge is usually profuse, and remains so during 
several days, then showing gradual diminution, and finally, in favorable 
cases, ceasing altogether at the end of a period varying from one to thiee 
or four weeks. 

The distinguishing features of the discharge in acute otitis media are 
explained by the fact that they depend upon a lesion characterized by 
absence of bone necrosis, and which shows a marked tendency to self- 
limitation. Hence the absence of odor, and the gradual cessation. 

Discharge in Chronic Suppurative Otitis. d he discharge in 
chronic middle-ear suppuration may be very profuse or so scanty that the 
patient may be quite ignorant of its presence. Lsually it is subject to 
variations in this respect, being at times exceedingly profuse and at other 
times barely noticeable. Rarely does it disappear wholly, however, inspec¬ 
tion by reflected light showing more or less destruction of the drum mem¬ 
brane and a granulating surface in the depths of the tympanic space, from 
which foul-smelling pus may be removed by means of a cotton-wound 
applicator. The odor also varies, being in some cases unbearably offensive 
and a source of unhappiness to the patient and in others of a sickening but 
less pronounced character noticeable only when removed from the depths 

of the canal. „ . . 

These, then, are the characteristic features of the discharge in chronic 

middle-ear suppuration,—viz. (1) its constant odor and (2) its persistency. 
As in the case of acute otitis media, the character of the discharge is ex- 


136 


SUBJECTIVE SYMPTOMS OF AUEAL DISEASE 


plained by the character of the lesion,— i.e., its odor being due to the 
presence either of carious bone or of necrotic epithelial elements, and its 
persistency to the progressive character of the disease, which, though 
quiescent at times, tends rather to further extension and involvement of 
adjacent structures than to final resolution. 

In acute otitis media the appearance of an offensive odor in the dis¬ 
charge usually means either gross neglect—the pus being allowed to remain 
for days in the canal—or a change in the character of the lesion— i.e., 
chronicity due to bone caries. 

In chronic suppurative otitis media, complete and permanent disap¬ 
pearance of odor from the discharge would suggest possible elimination of 
the necrotic bone, which occasionally is thrown off in the form of minute 
sequestra in the pus, thus paving the way for final resolution. Such 
spontaneous cures undoubtedly occur. 

Tinnitus Aurium.— Of all the symptoms which the aurist is called 
upon to relieve, tinnitus aurium is the most elusive and difficult to control. 
It may be caused by any form of tympanic or labyrinthine disease, and 
may result from other conditions not dependent upon disease of the 
auditory apparatus. We may cure a tympanic lesion, but fail to relieve 
the tinnitus. This is a disappointing experience which every aurist has 
met with. 

In some cases tinnitus is the only symptom of which the patient is 
conscious, and there may be little else that is abnormal either in the physi¬ 
cal or the functional condition of the ear. So baffling may such cases prove 
that it may not be amiss to devote some space to a theoretic discussion of 
the various conditions which may give rise to this elusive symptom. 

Obviously the most useful classification of the different forms of tin¬ 
nitus aurium would be one based upon the underlying lesions or disorders. 
I believe that most cases will be found to fall under one or other of the 
following heads: 

1. Obstruction sounds, or noises due to occlusion or impaired mobility 
of some portion of the sound-conducting apparatus. 

2. Blood sounds, or noises produced by the blood current in vessels in 
or near the ear, and due either to disturbances of the local or general circu¬ 
lation, or to abnormalities in the size, shape, or position of the vessels. 

3. Labyrinthine sounds, or noises due either to structural changes in 
the cochlea, or to alterations—either increase or diminution—of intra- 
labyrinthine pressure. 

4. Neurotic sounds, or noises due to abnormal irritability of the audi¬ 
tory nerve. 

5. Cerebral sounds, or noises due to abnormal conditions acting upon 
the auditory centres in the cerebral cortex. 

Obstruction Sounds. —Under this general term we may include the 
numerous cases in which tinnitus aurium can be traced to its cause in a 
demonstrable lesion of the sound-conducting apparatus. In acute tubal 
catarrh, two symptoms chiefly engage the patient’s attention,—viz., 


TINNITUS AURIUM 


137 


impaired hearing and tinnitus,—and both disappear as the function of 
the tube is re-established. Again, in acute purulent otitis media, after 
the pain has been relieved by incision or rupture of the drum membrane, 
three symptoms continue to disturb the patient,—viz., impaired hearing, 
the discharge, and tinnitus aurium,—and all of them may disappear as 
resolution advances. In such cases the evidence is apparently conclusive 
that the subjective sounds are the direct result of a disturbed balance of 
the conducting apparatus. In studying these simpler forms of tinnitus, 
Panse advanced the theory that the function of the conducting apparatus 
is not only the transmission of sound waves to the ear, but also the con¬ 
duction from the ear of sounds which otherwise would act too strongly 
upon the perceptive mechanism. As supporting this hypothesis, he quoted 
the statement of von Troltsch 1 that “all noises actually arising in or near 
the ear must necessarily act more strongly on the auditory nerve if the 
natural outward sound conduction be in any way diminished.” 

Another way of explaining this form of tinnitus would be to state 
that there are always present in the neighborhood of the healthy ear sono¬ 
rous vibrations due to certain physiological processes— e.g., the blood cur¬ 
rent—which normally do not reach the inner ear; that such vibrations, 
when they do reach the perceptive mechanism, must do so by bone con¬ 
duction; that bone conduction is always increased when the mobility of 
the ossicular chain is impaired; and, therefore, that sounds accompanying 
the simpler middle-ear lesions are in many cases the result of normal 
sonorous vibrations, which by reason of increased bone conduction are 
permitted to reach and impress the end organs of the auditory nerve. 
Have a vibrating tuning-fork held in contact with the median line of the 
skull, until its vibrations cease to be appreciated as sound. It is still 
vibrating, but now so feebly that the sound is no longer heard. Now close 
both ears by a finger pressed in each meatus, and the sound of the still vi¬ 
brating fork is again distinctly heard, and now also another sound is heard 
which is produced by the normal blood current in vessels in or near the ear. 
In other words, we have blocked the natural outward pathway of sound 
conduction, with the result that vibrations normally imperceptible pass by 
bone conduction to the perceptive mechanism and are appreciated as sound. 

It would seem that this theory of the causation of tinnitus might be 
found to apply to certain sounds for which other causes are sometimes 
assigned. For instance, it has frequently been noted, that, when the eyes 
are tightly closed by strongly contracting the orbicularis palpebrarum 
muscles, a low, buzzing sound is heard. This is supposed to be due to a 
sympathetic contraction of the stapedius, and is commonly spoken of as a 
“muscle sound.” But if we will produce this sound by forcibly closing 
the eyes, and then compare it with the sound produced by placing a finger 
lightly in each external auditory meatus, we shall find that the two sounds 
are very similar in quality and pitch, though the latter is of greater inten- 


1 Von Troltsch: cited by Panse, Arch, of Otol., vol. xxviii, p. 365. 





138 


SUBJECTIVE SYMPTOMS OF AUEAL DISEASE 


sity. May not this so-called muscle sound be thought of more correctly 
as a conduction sound, and as due to a temporary interference with out¬ 
ward sound conduction, during the contraction—which lasts but a few 
moments—of the stapedius muscle? 

Since tympanic lesions may be accompanied by a high degree of con¬ 
gestion and, by pressing the stapes inward, may produce changes of the 
intra-labyrinthine pressure,, it is evident that all cases of tympanic tin¬ 
nitus do not necessarily belong to this class. That is, there may be other 
causative factors at work. 

The outward conduction of sound may be interfered with by anything 
which occludes the meatus,— e.g., cerumen, foreign body, furuncle, etc.,— 
or by anything which interferes with the mobility of the ossicular chain,— 
e.g., tubal catarrh with retraction of the drum membrane, tubotympanic 
congestion, fluid effusions within the tympanic cavity, constricting bands 
binding the ossicles together or to the tympanic walls, etc., etc. 

Viewed in this way, it is quite logical to treat these conditions locally 
and expect the tinnitus to subside as the parts regain their normal condition. 

Blood Sounds. —The so-called blood sounds may be of arterial or 
venous origin. They may be dependent upon anatomical anomalies and 
not upon any pathological condition, in which case they are not to be 
looked upon as a symptom of disease, and are often not amenable to treat¬ 
ment. The close relation, for example, of the internal carotid, artery and 
the internal jugular vein to the tympanum is well known. The anterior 
wall of the tympanum is separated from the internal carotid by a thin 
bony plate only, and the tympanic floor is in relation with the jugular 
fossa, which lodges the bulb of the jugular vein. As an abnormal congenital 
condition the carotid canal may project into and encroach upon the cavity 
of the tympanum, and it is not difficult to conceive that any malposition 
in this direction might give rise to sounds which the patient could not fail 
to hear. In the tympanic floor, also, dehiscences may exist either as a 
congenital defect or as a result of an old necrotic process which has under¬ 
gone resolution. Many such cases have been observed during surgical 
operations and in the course of post-mortem examinations. At a meeting 
of German naturalists many years ago, Professor Korner , 2 of Rostock, 
presented, among other specimens, a temporal bone showing a fissure in 
the tympanic wall of the carotid canal. Dr. Dench 3 has recorded the case 
of a young woman upon whom he performed the operation of ossiculec¬ 
tomy. After removal of the ossicles, “a bluish mass was seen in the floor 
of the tympanum, which proved to be the bulb of the jugular vein, its 
exposure being due to a defect in the tympanic floor.” 

These cases are not unique, and are cited simply to emphasize the 
fact that tinnitus is not necessarily an evidence of disease. They cor¬ 
roborate the statement of Schwartze , 4 that “continuous noises may occur 

2 Korner: Arch, of OtoL, vol. xxxi, p. 119. 

3 Dench: Arch, of OtoL, vol. xxvii, p. 297. 

4 Schwartze: cited by Panse, Arch, of OtoL, vol. xxviii, p. 354. 




TINNITUS AURIUM 


139 


during a lifetime in persons of normal hearing, due probably to anomalies 
in the course of vessels.” 

A persistent form of tinnitus, which we may also assume to indicate 
circulatory derangement, is that which may accompany visceral disturb¬ 
ances in other parts of the body. It is a well-recognized fact that visceral 
disorders—notably disorders of the pelvic and abdominal viscera—fre¬ 
quently produce aural symptoms. Woakes 5 explains this on the hypothesis 
of a nervous relationship between the viscera in question and the laby¬ 
rinth. He points out that the nerves regulating the calibre of the vertebral 
arteries, and also of the basilar artery and its branches, including the 
internal auditory which supplies the labyrinth, come from the inferior 
cervical ganglion of the sympathetic. The stomach and other abdominal 
viscera are largely supplied by the pneumogastric nerves, and the com¬ 
munication between the vagus and the inferior cervical ganglion is estab¬ 
lished by means of a fasciculus from the vagus to the ganglion in question. 
Thus, in certain disorders of the stomach, for instance, impulses may be 
sent by way of the inferior cervical ganglion to the labyrinth, whereby 
its arteries are caused to dilate. Woakes claims that under such conditions 
the blood supply to the area involved “may be ten times as great as ” under 
normal conditions. With this theory in mind it is no tax upon our cre¬ 
dulity to accept the statement that “cases of tinnitus from constipation, 
subacute gastritis, and pathological conditions within the pelvis are of 
common occurrence.” 

In such cases it would be logical to expect the tinnitus to yield to treat¬ 
ment directed against the existing visceral disorders. 

Patients with chronic endocarditis form another class who occasionally 
suffer with tinnitus. TV hen with chronic valvular disease a murmur heard 
objectively at the base of the heart is transmitted to the vessels of the 
neck, an accompanying tinnitus may be clearly due to transmission ol the 
cardiac murmur. Strumpel , 6 7 in writing of aortic regurgitation, speaks 
of cases in which, “ by applying a stethoscope lightly over the femoral, 
the brachial, and often over the radial and ulnar arteries, a marked valvu¬ 
lar sound” is heard. It would be surprising if such a murmur were not 
transmitted also to the patient’s organ of hearing. A peculiarity of this 
variety of tinnitus is the fact that in some cases the sound heard by the 
patient may be heard also by the physician through the otoscope. As 
illustrating this statement may be mentioned the case of Spiiig, cited by 
Panse. His patient, a sufferer from aortic regurgitation, was troubled by 
subjective noises, at first pulsating, later becoming continuous. Objec¬ 
tively it was heard through the otoscope on the right side, a rhythmic, 
blowing sound: and a similar sound was heard through the stethoscope 
over the aorta, right carotid, subclavian, and brachial arteries. 


6 Woakes: Deafness, Giddiness, and Noises, p. 135. 

6 Strumpel: System of Medicine, p. 289. 

7 Spirig: cited by Panse, Arch, of Otol., vol. xxviii, p. 371. 






140 


SUBJECTIVE SYMPTOMS OF AURAL DISEASE 


Another variety of subjective blood sounds which in rare cases may be 
heard by the physician through the otoscope is that which occurs with 
intracranial aneurisms. The basilar and internal auditory arteries are the 
vessels said to be most often affected. Excluding, then, a transmitted 
cardiac murmur, a pulsating noise synchronous with the pulse, heard sub¬ 
jectively and objectively in both ears, would suggest aneurism of the 
basilar artery; if heard only in one ear, the inference would be of aneurism 
of the corresponding internal auditory artery. Obviously, in such cases 
the tinnitus is not amenable to treatment except in so far as cardiac and 
nerve sedatives may lessen its intensity. 

Blood sounds are usually of low or medium pitch, and are diagnosti¬ 
cated by their character and by the exclusion of other causes. Pulsating 
noises are of arterial origin, whereas venous sounds are uniform or non¬ 
pulsating in character. 

There should also be mentioned a venous blood sound, which sometimes 
occurs with chronic or long-continued anaemia. It is a low, continuous 
hum, supposed to be due to the altered condition of the blood in its pas¬ 
sage from the sinus into the bulb of the jugular vein. This sound is prob¬ 
ably somewhat analogous etiologically to the haemic bruit which in anaemia 
is sometimes heard objectively over the large veins of the neck, the so- 
called bruit du diable. The diagnosis depends upon the character of the 
sound, the absence of tympanic disease, exclusion by functional tests of 
labyrinthine disease, and evidences of anaemia as shown by the general 
symptoms and examination of the blood. Obviously the indications would 
be for iron, arsenic, tonics, or any treatment looking to the restoration of 
the blood to its normal condition. 

Labyrinthine Sounds. —That subjective noises are invariably present 
at the onset of acute suppurative labyrinthitis is a fact universally recog¬ 
nized. This, however, is a class of cases in which by comparison with 
other more distressing phenomena, the tinnitus becomes a minor symp¬ 
tom. The subjective noises accompanying suppurative labyrinthitis will 
not be considered in this chapter. 

There are, however, many cases of chronic non-suppurative middle- 
ear disease in which the accompanying tinnitus seems hardly to be ex¬ 
plained as resulting from the tympanic changes alone. There are, for 
example, cases in which every known local therapeutic measure may be 
employed without in the slightest degree influencing the subjective noises. 

In our study of such cases, we must remember that the auditory nerve 
not only receives and transmits sound impressions in response to sonorous 
vibrations (its normal function), but may also convey noise impulses to 
the auditory centres purely as a result of irritation or disturbance of its 
terminal cochlear fibres (perversion of function). 

Many investigators (Grant , 8 Politzer , 9 Gruber 10 ) have placed both 

8 Grant, Dundas: The Clinical Journal (London), vol. ix, pp. 241-7. 

9 Politzer: Diseases of the Ear, pp. 622-5. 

10 Gruber: Diseases of the Ear, p. 514. 





TINNITUS AURIUM 


141 


congestion and anaemia of the labyrinth among the causes of tinnitus. 
George R. Field 11 over thirty years ago emphasized his conclusion that 
“ slight variations, either of increase or diminution, in the pressure on 
the delicate structures (of the labyrinth) may give rise to severe tinnitus.” 
There is much clinical and some experimental support of this view. Ani¬ 
mals killed after frequently repeated doses of quinine, salicylic acid, etc., 
have shown marked labyrinthine congestion,—congestion sufficiently 
pronounced to have markedly increased intra-labyrinthine pressure; and 
these drugs in repeated doses usually cause distressing tinnitus in man. 
Amyl nitrite is another drug which invariably causes loud tinnitus, and 
here the effect so rapidly follows the cause that it seems possible to explain 
it only by reference to the increase in intra-labyrinthine pressure which 
the drug undoubtedly induces. On the other hand, after severe hemor¬ 
rhage, when the patient lies in a condition bordering on collapse from a 
withdrawal of blood from all the tissues of the body, tinnitus is usually a 
prominent symptom, and in this case we are obliged to assume a reduction 
of intra-labyrinthine pressure. 

Granting, now, that congestive conditions of the middle ear may 
cause vascular disturbances within the labyrinth, we can easily conceive 
that the commoner hypertrophic, or hyperaemic, form of chronic catarrhal 
otitis media may, through anastomotic channels, cause and maintain a 
constant state of moderate labyrinthine congestion. 

It is a fact long known to pathologists that low grades of hypersemia, 
long continued, almost invariably give rise to morbid changes in the tis¬ 
sues involved. It is probable, therefore, that in cases of obstinate tinnitus 
apparently dependent upon chronic catarrhal otitis media, we have also 
to contend with certain structural changes within the labyrinth which, 
being beyond our reach, account in many cases for our failure to relieve 
the subjective sounds. I believe that in this form of tinnitus more can be 
accomplished by regulating the patient’s mode and habits of life, atten¬ 
tion to hygiene, and possibly by constitutional remedies, than by local 
treatment. 

Neurotic Sounds. —Those subjective noises may be classed as neu¬ 
rotic sounds which depend upon a hypersensitive condition of the auditory 
nerves. The tinnitus in most of these cases is to be regarded as a pure 
neurosis,— i.e., it is dependent upon a functional disorder of the nervous 
system in which the auditory nerves share and sympathize. They may 
present no evidence of organic disease, yet are shown to be in a condition 

of increased or abnormal irritability. 

This condition of acoustic hypersesthesia may be produced by toxic 
matters circulating in the blood, which act as irritants upon the auditory 
nerves. In this way may be explained the temporary tinnitus occurring 
in some cases of chronic Bright’s disease, also the tinnitus occurring 
occasionally without evidence of tympanic disease in the course of acute 
infectious d iseases. _________ 

11 Field: Medical Times and Gazette, June, 1878, p. 616. 





142 


SUBJECTIVE SYMPTOMS OF AURAL DISEASE 


The most characteristic cases of neurotic tinnitus , however, are found 
in patients suffering from neurasthenia or nervous exhaustion. In the 
diagnosis of these cases the process of exclusion naturally plays an impor¬ 
tant part. Thus, on examination of the patient, there may be found no 
disorder of the general circulation, no evidences of disturbed labyrinthine 
pressure, no visceral disorders which might affect the ear reflexly. Exam¬ 
ination of the ear may reveal nothing abnormal within the meatus or tym¬ 
panum, or, as is more common, a tympanic lesion being present, its correc¬ 
tion does not result in relief of the tinnitus. Such negative results should 
suggest, at least, the possibility of a functional nervous disorder. 

Careful questioning brings out the fact that the noise is made worse 
by bodily or mental fatigue; thus, it may be absent or hardly noticeable 
in the morning, after a night’s rest, but reappears or becomes distressing 
as the day advances. 

On functional examination, the hearing may at first seem nearly or 
quite normal. The tone limits are well maintained; lower tone limit nor¬ 
mal, upper tone limit unchanged, or may be raised. For certain sounds 
usually the higher notes of the musical scale, and such sharp sounds as 
are produced by the watch and acoumeter—the hearing may be abnor¬ 
mally acute,— i.e., those sounds may be perceived further than the normal 
hearing distance. 

But while the patient’s hearing power may be normal, or even hyper¬ 
acute at certain times, it will usually be found to show great variations, 
and to suffer rapid diminution as the patient becomes fatigued. Thus, 
the hearing power may be very much better in the morning than in the 
late afternoon after the fatigues of the day. 

It is also characteristic of these cases (Dench 12 ) that the patient may 
hear very well when conversing with one person, but with great difficulty 
when engaged in general conversation, the mental effort necessary to this 
attempt resulting in fatigue, which quickly reacts upon the auditory 
nerves. 

Dundas Grant 13 has recorded some interesting cases of tinnitus due to 
nervous exhaustion. Having excluded tympanic lesions and the more 
usual constitutional causes, he made careful inquiry into the patient’s 
habits, and in many cases elicited a history of overwork, prolonged anxiety, 
alcoholism, dissipation, sexual excess, or of some mode of life logically 
leading to nervous breakdown. Following up this clue, he found on 
functional examination marked hyperacusis,—a vibrating tuning-fork 
held opposite the patient’s ear being heard twice the normal period of 
time, and the watch-tick being heard in some cases “across the room.” 
In many of these cases the tinnitus was relieved only by regulation of the 
patient’s life and by treatment appropriate to his nervous disorder. 

Dana 14 places neurasthenia among the chief factors in the causation of 

12 Dench: Diseases of the Ear, p. 605. 

13 Grant: Loc. cit. 

14 Dana: Nervous Diseases, p. 188. 



TINNITUS AUEIUM 


143 


tinnitus. He defines neurasthenia as a Afunctional nervous disorder, 
which is characterized by an excessive nervous weakness and nervous 
irritability, so that the patient is exhausted by slight causes and reacts to 
slight irritation.” 

W ith this definition in mind, it becomes evident that the aural symp¬ 
toms are the logical results of the disease; that the tinnitus and hvper- 
acusis are due to the “nervous irritability,” while the variations of the 

hearing power under the influence of fatigue are due to the “nervous 
weakness.” 

It is probable that there are many cases of tinnitus of mixed origin in 
which the neurotic element is masked by other causative elements more on 
the surface; e.g., a tympanic lesion, tubal catarrh, etc. It is the opinion 
of the writer that cases of tinnitus belonging, at least partially, to this 
class are far more common, even among the laboring classes, than is usually 
supposed. For, while neurasthenia is commonly supposed to be a disease 
to which brain workers and so-called upper classes are particularly prone, 
we have Dr. Dana’s authority for the statement that sufferers among 
laborers and artisans are by no means uncommon. 

Cerebral sounds, or sounds due to irritation of the auditory centres 
in the cerebral cortex, may be dealt with briefly. 

This form of tinnitus is not very common in otological practice, and is 
of interest as much to the neurologist as to the otologist. Most authori¬ 
ties agree that complex or elaborated sounds— i.e., sounds taking the form 
of voices, tunes, distinct words or sentences—are to be regarded as of 
cerebral origin. 

The subjective noises which epileptics experience as a warning of 
impending attacks must also be regarded as due to a central lesion; and it 
is perhaps important to recognize this premonitory symptom from the fact 
that its presence is thought to bear somewhat on the prognosis of epilepsy, 
and to be of ill omen. Gowers 15 refers to the fact that “epileptics with 
such an aura are in greater danger than others of becoming insane.” The 
hearing of complex or elaborated sounds is also believed by many to carry 
with it an unfavorable prognosis. While it is generally believed that the 
hearing of elaborated sounds points to irritation of the cerebral auditory 
centres, there are others who hold further that this symptom is an evidence 
of mental instability. Thus, Gruber 16 states that “patients who hear 
human voices, words, conversations, etc., are either mentally diseased or 
become so later.” It seems hardly justifiable, therefore, to regard such 
subjective phenomena as aural symptoms, and as otological text-books 
and literature throw little, if any, light on the proper method of treatment, 
it would seem to be for the best interests of such patients to refer them to a 
competent neurologist. 

In trying to differentiate the various forms of tinnitus in accordance 


15 Gowers: British Medical Journal, Nov. 14, 1896. 

16 Gruber: Diseases of the Ear, p. 547. 



144 


SUBJECTIVE SYMPTOMS OF AURAL DISEASE 


with the underlying causes, we have the following sources of information 
to draw from: 

1. Evidences of disease in any portion of the conducting apparatus 
as shown by physical examination. 

2. History of the case, and character of the sound, as described by 
the patient. 

3. Results elicited by careful functional examination. 

4. Evidences of disease in other parts of the body, particularly as to 
the presence of digestive disorders, circulatory disturbances, blood dys- 
crasias, or disease of the nervous system. 

5. Effect of certain drugs, either in relieving or aggravating the 
tinnitus. 

The importance of a careful physical examination of the ear becomes 
evident from the fact that any appreciable lesion in any portion of the 
conducting apparatus must act at least as a contributing cause in the 
production of tinnitus, whatever the character of the sound and whatever 
the chief factor in its causation may be. 


CHAPTER VII. 


ACUTE INFLAMMATORY DISEASES OF THE EUSTACHIAN TUBE, 

MIDDLE EAR, AND MASTOID PROCESS. 

Acute Tubal Catarrh; Eustachian Catarrh; Tubotympanic 
Congestion.—Tubal catarrh is the precursor of almost every form of 
tympanic disease, and as such deserves a more prominent place than 
is usually accorded it among diseases of the sound-conducting apparatus. 
It may be defined as an acute inflammation of the Eustachian mucosa, 
which may or may not give rise to aural symptoms, according to 
whether the lumen of the canal is, or is not, occluded thereby. 

Etiology". —Among predisposing causes must be included all condi¬ 
tions interfering with normal nasal respiration. The presence of post¬ 
nasal adenoids is, therefore, a particularly potent factor, and children are 
much more frequently sufferers from tubal congestion and inflammation 
than is generally recognizedA Among adults such obstructive lesions as 
hypertrophic rhinitis, septal deflections, ecchondroses and exostoses of the 
septum, etc., are conditions which are apt to induce recurrent attacks of 
Eustachian catarrh. Of exciting causes by far the most frequent and 
important is the common “cold in the head,” or acute rhinitis, with which 
some degree of Eustachian congestion or inflammation is probably always 
associated. 

Pathology . 1 —In a first attack of acute tubal inflammation the lesion 
is probably in most cases confined to the membrano-cartilaginous, or 
pharyngeal, portion of the canal. Beginning as a simple venous congestion, 
the condition is later converted into an acute exudative inflammation. In 
the great majority of cases it is probable that the lesion never advances 
to the point of actual tubal obstruction, in which case the tubal functions 
may not be seriously disturbed, and aural symptoms are slight or absent. 
The tube may, however, be occluded in one of two ways, viz. (a) inflam¬ 
matory swelling of the parts about the pharyngeal orifice may by pressure 
close the canal at this point, or (b) the inflammatory changes may extend 
into the osseous portion of the canal, obliterating its lumen at the isthmus. 

Tympanic Changes .—So long as the Eustachian canal remains patent, 
or, rather, so long as it continues to perform its function of supplying air 
to the tympanic cavity, no changes are observed in the drum membrane. 
As soon, however, as the tubal function is disturbed,— i.e., when the supply 
of air to the tympanum is diminished,—the air pressure within the middle- 
ear cavity becomes negative, and more or less congestion of the tympanic 


1 Our knowledge of the morbid changes characterizing this lesion is based largely 
upon conditions actually demonstrable during the onset and height of the attack, and 
their analogy with similar processes elsewhere in the body. 

10 


145 






146 ACUTE DISEASES OF MIDDLE EAR AND MASTOID 


vessels ensues. This probably explains the prodromal symptom,—the 
feeling of occlusion or “stuffiness in the ear,” which is sometimes com¬ 
plained of. When finally the Eustachian canal is completely occluded, 
the drum membrane is forced inward toward the inner tympanic wall by 
the unopposed atmospheric pressure from without. Inspection of the ear 
may now reveal the picture of a drum membrane showing no color or 
structural changes, but greatly retracted. It is probably at this point that 
the onset of aural symptoms is usually experienced. 

Unless the tubal lesion is promptly controlled, very marked congestion 
of the tympanic mucous membrane may occur, and the peripheral plexus 
of veins along the margins of the drum membrane and the attachment of 
the hammer handle will be greatly engorged. This condition is described 
in some text-books as a distinct lesion under the name of tubotympanic 
congestion. It in reality constitutes a later stage of an acute tubal in¬ 
flammation, and is a logical result of the lesion when unusually severe and 
prolonged. 

Symptoms. —As before stated, complete absence of aural symptoms 
is by no means inconsistent with moderate grades of tubal catarrh. It is 
probable, therefore, that most of us are occasional sufferers from this 
lesion without experiencing symptoms referable to the ear. When occlu¬ 
sion of the canal gives rise to tympanic disturbance, the symptoms usually 
present themselves somewhat in the following order: 

In a certain proportion of cases the attack is ushered in by a feeling of 
occlusion of the ear. This rather indefinite symptom is variously described 
by patients as a sensation of “stuffiness,” or closure of the ear, or of the 
presence of a foreign body in the canal. This may persist for a few days 
and then disappear as the canal regains its normal condition; or it maybe 
the forerunner of more definite symptoms of functional disturbance. 

More commonly, according to the writer’s experience, the first symp¬ 
tom complained of is that of marked impairment of hearing. This is often 
the more noticeable and distressing from its sudden development. The 
deafness is of the type characteristic of disease in any part of the conduct¬ 
ing apparatus. Functional tests show diminished hearing for the watch, 
acoumeter, and for the conversational voice and whisper. Hearing for the 
lower musical tones is noticeably lessened, the upper tone limit not being 
disturbed. Hearing by bone conduction is always increased. 

With the impairment of hearing the patient usually experiences rather 
loud subjective sounds, or tinnitus aurium. The noise usually is of high 
pitch, and is variously compared to the sound of a cricket, the escaping of 
steam, the noise of a shell against the ear, the sound of the surf, the ring¬ 
ing of bells, etc., etc. Quite often there is evident difficulty in recalling 
any natural sound with which to compare it. 

In exceptional cases there is slight subjective vertigo, usually lasting 
but a few seconds, and rarely or never sufficiently pronounced to disturb 
static equilibrium. This symptom, when present, is presumably due to 
disturbance of intra-labyrinthine pressure, brought about through retrac- 


ACUTE TUBAL CATARRH 


147 


tion of the drum membrane and inward pressure upon the ossicular chain 
and foot-plate of the stapes. 

Aural pain is usually absent, practically always so during the first 
stage of tympanic disturbance from tubal catarrh. There are no consti¬ 
tutional symptoms,— e.g., fever, pulse changes, etc.,—unless such are 
present as a result of intercurrent disorder, or of the disease to which 
the tubal catarrh is secondary,— e.g., acute rhinopharyngitis, tonsillitis, 
grippe, etc. 

Physical Signs. —Following the onset of aural symptoms, inspection 
by reflected light usually shows a drum membrane which is more or less 
retracted but otherwise normal. Since one of the most difficult tasks for 
the beginner is the detection of moderate degrees of retraction, it may be 
well to speak here of the changes in its physical appearance which usually 
characterize this condition. Extreme retraction, such as occasionally 
occurs in the presence of marked atrophy and loss of tension of the mem- 
bran a tensa, is characterized by such obvious ballooning of the membrane 
inward and away from its points of attachment as to be easily recognizable 
even by the beginner. This, however, is an exceptional condition, such 
extreme displacement of the whole membrane being ordinarily prevented by 
the resistance which its inherent strength offers to the atmospheric pres¬ 
sure from without. It is quite important, therefore, that one should be 
able to recognize the moderate grades of retraction which are the more 
usual result of partial occlusion of the tube. 

Cardinal Signs of Retraction—Hammer Handle .—It will be remembered 
that the drum membrane is obliquely placed at the fundus of the bony canal, 
its outer surface looking outward and also strongly downward and forward. 
When yielding to pressure from without, it moves inward, backward, and 
upward, carrying the hammer handle with it. As seen through the canal, 
the hammer handle appears shorter and having a more decidedly back¬ 
ward direction than normally. This foreshortening of the hammer handle 
is in some cases extremely pronounced, and is one of the characteristic 

signs of a retracted drum membrane (Fig. 94). 

There are certain cases, however, in which the distance between the 
umbo and the promontory is so small that the hammer handle is pre¬ 
vented from any extensive inward displacement. Under such conditions, 
while occupjdng very nearly its normal position, it is apt to appear ab¬ 
normally broad and prominent from the fact that the dium membrane in 
moving inward is more or less folded about it (Fig. 96). 

Processus Brevis .—The short process projects from just below the nc ck 
of the malleus in a direction both outward and upward. It is held firmh 
in position by the anterior and posterior ligaments (axis band), which are 
attached to the malleus a little below the level of the upper surface or 
point of the short process. In retraction of the drum membrane, the 
hammer handle moves inward, while the short process rotates outwaid. 
The short process appears, therefore, more prominent, as it realty is, than 
when the membrana tensa occupies its normal position. Unusual prom- 


148 ACUTE DISEASES OF MIDDLE EAE AND MASTOID 


inence of the short process constitutes a second sign of retraction (Figs. 
94 and 95). 

Light Reflex .—It will be recalled that this phenomenon of the normal 
drum membrane is due not to any structural change at this point, but 
simply to the fact that the drum membrane within this particular space 
falls into a plane which reflects the light directly upon the eye of the 
examiner. It is obvious, therefore, that with any change in the position of 
the lower part of the tense membrane, either the light reflex must be lost 
or its form changed. It may appear as a single, minute, shining spot 
immediately in front of the umbo (Fig. 94), or may be divided into two or 
more points of light. A common type of divided light reflex resulting from 





■MBa, 





Fig. 94.—Retracted drum 
membrane. 


Fig. 95. — Retracted drum 
membrane. 


Fig. 96. — Retracted drum 
membrane. 


retraction occurs as a minute point of light in front of the umbo, and a 
second crescentic reflex lying near and parallel with the lower anterior arc 
of the annulus tendinosus (Fig. 95). 

Another characteristic sign of retraction, which may be difficult to 
recognize in slight degrees of retraction, but is easily noticeable in cases of 
marked displacement, is due to the fact that the drum membrane is drawn 
away from the structures to which it is attached, causing them to appear 
unusually prominent. Thus, the annulus tympanicus, the anterior and 
posterior folds and the hammer handle, when this structure is not greatly 
foreshortened, stand out in exaggerated prominence. This condition is 
fairly well indicated in Fig. 96. 

To epitomize: the cardinal signs of a retracted drum membrane are: 

1. (a) Foreshortening and rotation backward of the manubrium mallei, 
or (b) apparent thickening and undue prominence of the same. 

2. Unusual prominence of the short process. 

3. Absence, or changes in the form, of the light reflex. 

4. The anterior and posterior folds and the annulus tendinosus appear 
unusually prominent. 

The Course of the Disease. —According to the development of 
tympanic changes, the disease may follow one of three roads toward final 
recovery. 

1. In favorable cases the symptoms may last but a few days, disap- 













TREATMENT OF TUBAL CATARRH 


149 


pearing completely as the tubal inflammation subsides and the canal 
regains its normal calibre. 

2. In cases of delayed resolution, the negative air pressure within the 
middle-ear cavity may result in very marked congestion of the mucous 
membrane lining the tympanum. This condition is usually characterized 
by-engorgement of the venous plexus which is situated along the periphery 
of the drum membrane and along the margins of the hammer handle. 
The drum membrane, therefore, exhibits a line of redness in these regions,— 
i.e., along the edges of the drum membrane and hammer handle. This 
marginal redness varies in intensity in different cases, but always preserves 
the characteristic of being differentiated by a distinct line of demarcation 
from the central area of normal membrane (Fig. 97). 

The symptoms are those described as belonging to 
the earlier stage of tubal catarrh, with the difference 
that aural pain (earache) may be present. It may, 
however, be absent, and when present is not usually 
very severe. This condition is spoken of by some 
authors as “tubotympanic congestion,” a very use¬ 
ful and descriptive name, which should not, how¬ 
ever, lead us into the error of regarding it as a 
separate lesion. The tympanic condition and ac¬ 
companying symptoms usually subside as the tubal 
inflammation undergoes resolution. 

3. There is still a third possibility in the conversion of the tym¬ 
panic congestion into a simple acute inflammation with effusion of 
serum into the middle-ear cavity. This constitutes the purest form 
of acute catarrhal otitis media, as distinguished from acute purulent 
otitis media. 

Prognosis. —Acute tubal catarrh— i.e., in the first few attacks—tends 
to spontaneous and complete recovery. Frequent recurrence of tubal 
inflammation gives rise to chronic catarrhal conditions within the middle- 
ear cavity, leading to impairment of hearing later in life. 

Treatment. —The treatment of tubal catarrh may be directed along 
three lines—viz., (a) internal and local remedies intended to relieve naso¬ 
pharyngeal congestion, (b) local treatment of the tube aiming to re-estab¬ 
lish its function, and (c) correction of nasal and nasopharyngeal lesions 
which might act as influences toward recurrence. 

Treatvient of the Nasophary?ix .—In the first place, if the tubal lesion is 
very acute and accompanied by pronounced symptoms ol nasopharyngeal 
congestion,— i.e., those of a common “cold,”—the logical treatment is by 
active measures to combat the latter condition. Therefore, confining the 
patient to bed, brisk catharsis, and repeated small doses of quinine will 
do much to shorten the attack. 

Even when it is not practical to carry out these measures, or when the 
symptoms do not seem to warrant them, much can be accomplished by 
the internal administration of appropriate drugs. Thus, quinine in gram 



Fig. 97. — Tubo - tympanic 
congestion. 




150 ACUTE DISEASES OF MIDDLE EAR AND MASTOID 


closes repeated every three hours during the day, or three times daily, may 
aid materially in shortening the attack. Personally the writer believes in 
the use of atropine or belladonna in acute tubal catarrh, their value being 
clearly traceable to their blennostatic action upon the nasopharyngeal 
and tubal mucous membrane. Belladonna may be prescribed with advan¬ 
tage in the form of the well-known “rhinitis tablets,” Lincoln’s formula, 2 
half strength; or the extract of belladonna in gr. % doses may be combined 
with any of the coal-tar preparations. When the patient, in addition to 
characteristic tubal symptoms, exhibits the malaise and constitutional 
depression suggestive of grippe, or marked evidences of acute rhinopharyn¬ 
gitis, the following prescription will be found of great value,—particularly 
if the patient can be confined to bed for a few days. 

R Capsules or powders, each to contain: 

Extract, belladonnae, gr. 

Phenacetini, 

Salol, aa gr. iiss. 

Sig.—One capsule (or powder) every four hours. 

As with acute rhinitis, acute tubal catarrh may often at the onset be 
aborted by the timely use of appropriate drugs. After it has progressed 
beyond a certain stage, it must run its course, and the best that may be 
hoped for from internal medication is that the attack may be shortened 
thereby. 

Locally, spraying the nose and throat night and morning with a cleans¬ 
ing alkaline solution (e.g., Dobell’s solution, 3 glycothymolin, etc.) seems 
in some cases to exert a favorable influence. Alkalol is a proprietary 
preparation which answers this purpose nicely, and has the considerable 
advantage of being practically non-irritating. 

Certain cases of pronounced and intractable nasopharyngeal con¬ 
gestion or inflammation will respond favorably to a few repetitions of 
the following treatment: The nose and nasopharynx are thoroughly 
sprayed with a 5 per cent, solution of argyrol. This is allowed to remain 
a few minutes, and then washed out by means of the postnasal syringe 
with a warm normal saline solution. 

If the writer has dealt at some length with the treatment of the naso* 
pharynx, it must be remembered that the tubal inflammation is usually 
but an extension of a nasopharyngeal catarrh, and that whatever relieves 
the latter will provide the most logical treatment for the tubal lesion. 

Inflation .—The first step in the direct treatment of the tube is by some 


2 Lincoln’s “rhinitis tablets,” half strength, contain each: Extract. belladonnae gr. %, 
camphor, gr. %, and quininae sulphat. gr. %. 

3 Dobell’s solution: 

R Acid, carbolici, gr. iv; 

Sodii bicarbonat. 

Sodii borat., aa gr xl; 

Glycerini, oz. j; 

Aquae, q.s. ad oz. iv. 






TREATMENT OF TUBAL CATARRH 


151 


form of inflation. \\ hile this may be accomplished by the Politzer method, 
the catheter possesses the following considerable advantages: (1) We are 
able to inflate each ear singly and to regulate the pressure according to 
the resistance met with; (2) we obtain much more definite information as 
to the tubal condition from the clearer ausculatory signs ( i.e., through 
the otoscope); and (3) in our effort to force air through the more occluded 
tube, we are in no danger of unduly stretching the opposite drum mem¬ 
brane, as may easily occur in repeated Politzeration. 

Local Anaesthesia .—The routine use of cocaine is not either wise or 
necessary for patients whose treatment requires repeated catheterization. 
There can be no doubt that repeated use of cocaine for any purpose carries 
with it some danger of establishing the drug habit. On the other hand, 
patients are often more or less nervous during a first examination, and it 
may then be wise to eliminate the discomfort incident to catheterization 
by applying a weak solution of cocaine. It should not be used in the form 
of a nasal spray, which anaesthetizes a larger surface than is necessary, 
and is more apt to cause reactionary engorgement of all the nasal tissues 
than when the application is limited to the pathway to be traversed by the 
catheter. This is easily accomplished by passing a cotton-wound applica¬ 
tor (Fig. 99) which has been dipped in a 4 per cent, solution of cocaine, 
through the inferior meatus of the nasal cavity corresponding to the ear 
to be inflated. The cotton should be passed slowly back and forth three or 
four times. A minute or two thereafter, it will be found that the catheter 
can be passed through the nose without causing any discomfort. After 
this first catheterization, the use of cocaine should be altogether omitted. 

The technic of catheter inflation has already been described (pages 
65 69), and need not be repeated here. It is a procedure which with care 
and skill can be made practically painless, or in careless or unpractised 
hands may become a veritable ordeal to the patient. The catheter should 
find its way easily and without application of force through the inferior 
meatus, the attempt to force it past any obstacle encountered resulting 
not only in pain, but in injury to the tissues. When an obstacle is met with 
in some nasal abnormality,— e.g., a low 7 septal ecchondrosis or exostosis,— 
it is usually possible, by slowly rotating the catheter, to find a pathway 
along which the catheter will enter the nasopharynx without force. When 
this is not possible, catheter inflation will be of no benefit, and we should 
either resort to the Politzer method or subject the patient to preliminary 
operative treatment for the correction of the nasal lesion. The latter 
alternative will generally afford the shortest road to a permanent cure. 

Auscultatory Signs .—During inflation we may obtain important data 
as to the exact condition within the tubes from the sounds heard through 
the otoscope, or diagnostic tube. Thus, there may be (a) complete absence 
of sound characteristic of air entering the tympanum, this pointing to 
absolute occlusion of the canal; or (b) the presence of moist rales, changing 
in character, due to excessive secretion of mucus within the tube; or (c) 
the sound may be clearly indicative of air entering the tympanum, but 


152 ACUTE DISEASES OF MIDDLE EAR AND MASTOID 



fainter and of higher pitch owing to the reduced calibre of the canal, or, 

finally, (d) there may be bubbling rales char¬ 
acteristic of air passing through fluid, indicating 
the presence of serum in the lower part of the 
tympanic cavity. 

For all the above conditions, which are but 
stages or phases of the same lesion, the treat¬ 
ment is much the same. Inflation per catheter 
acts beneficially in several ways. Its first result 
is the re-establishment of the normal air pres¬ 
sure within the tympanum and the replacement 
of the drum membrane in its normal position. 
This frequently gives immediate relief of the 
symptoms, and in some cases restores the 
hearing almost to the normal standard. This improvement, how¬ 
ever, is often of very short duration, the discomfort and functional 
disturbance recurring as the air in the middle-ear cavity is again 
exhausted. Inflation seems also to act directly upon the tubal 
mucosa, restoring its tone and aiding in the removal of mucus 
accumulations which are brought away with the return air 
current into the nasopharynx. 

Inflation should at first be practised at short intervals,— 
i.e., daily or on alternate days,—and later at longer intervals. 
The improvement under this measure is often very rapid and is 
clearly indicated by the progressive changes in the character of 
the sounds heard through the otoscope. 

Local Application of Drugs. —There can be no doubt of 
the benefit in acute tubal catarrh from astringent applications 
to the pharyngeal mouth of the diseased tube. For this 
purpose the silver preparations give good results,— i.e., 
nitrate of silver in solution of gr. 10 to 20 to the ounce, or 
argyrol in 25 per cent, solution. They are best applied by 
means of a cotton-wound applicator, the end of which is 
made to describe a curve similar to that of the Eustachian 
catheter (Fig. 98). This is passed through the inferior mea¬ 
tus of the nose and rotated into the pharyngeal mouth 
of the tube by exactly the same manipulations as are employed 
in placing the Eustachian catheter. In my experience argy¬ 
rol is less irritating, and on the whole more effective, than 
the nitrate of silver. It can also be used more frequently,— i.e., 
twice or three times a week, — in appropriate cases, while 
nitrate of silver, even in weak solutions, should 
Fig. 98. —Eustachian no t be applied oftener than once in seven or eight 

cotton applicator. , A ,, , , . , . ™ . ° 

days. Another drug which is efficacious in some 
cases of Eustachian catarrh is the chloride of zinc in solution of gr. 
10 or gr. 20 to the ounce. 








TUBAL CATARRH IN CHILDREN 


153 


Treatment of Tubotympanic Congestion. —When the lesion has reached 
the stage described as tubotympanic congestion (Fig. 97), the necessity 
tor prompt therapeutic measures becomes urgent. Usually the treatment 
already outlined, but pushed rather more actively, will control the con¬ 
dition. Catheter inflation of the ear should be performed daily. The 
application of argyrol, in 25 per cent, solution, should be made to the 
nasopharynx and mouth of the tube on alternate days. Frequent gar¬ 
gling of the throat with alkaline or normal salt solution, as hot as patient 
can bear it, will in some cases act as a counter-irritant, relieving the tym¬ 
panic congestion. Extract of belladonna, gr. combined with small 
doses of quinine, repeated three times a day, or even four times daily, is 
of undoubted value in acute tubotympanic congestion. Earache, if severe, 
may be controlled by combining with the above an eighth of a grain 
of codeine for two or three doses. Finally, should the symptoms be 
aggravated by an effusion of serum within the tympanum, the best 
results will usually be obtained by a free incision through the posterior 
segment of the drum membrane. The incision is exactly the same as 
that to be described later under the treatment of acute catarrhal otitis 
media, and the subsequent cleansing of the canal must be carried out in 
the same way. 

Correction of Nasopharyngeal Abnormalities. — The acute symp¬ 
toms having subsided, it is of prime importance to the patient that 
the nose and nasopharynx should be carefully examined, and that 
any condition in this region interfering with nasal respiration or pro¬ 
vocative of nasopharyngeal congestion should be corrected. Probably 
much could be accomplished by the correction of such lesions not only in 
preventing the recurrence of acute tubal attacks, but also in the larger 
field of preventing subsequent impairment of hearing,— i.e ., deafness in 
later years. 

Tubal Catarrh in Children. —Before leaving this subject, the writer 
wishes to say a word as to the prevalence of tubal disease in young children. 

Of all the causes of tubal inflammation none is so potent or so wide¬ 
spread in the number of its victims as the presence of pharyngeal adenoids. 
The author has long been convinced that retraction or congestion of the 
drum membranes constitutes one of the most constant and reliable phys¬ 
ical signs of lymphoid hypertrophy in the nasopharynx; or, in other 
words, that the prevalence of tubotympanic disease in children is almost 
coequal with the prevalence of adenoids. If this view is correct, it is 
evident that the subject has not received due attention in otological 
literature and text-books, and, what is of more serious import, that the 
condition is more or less ignored or neglected by physicians and otologists 
alike. 

There are two predisposing causes which render children particularly 
prone to tubal congestion,—viz. (1) the greater prevalence of adenoids, 
and (2) certain anatomical characteristics of the Eustachian canal in 
infancy and early childhood. 


154 ACUTE DISEASES OF MIDDLE EAR AND MASTOID 


The more important anatomical differences between the infant and 
adult tubes are clearly indicated in Figs. 99 and 100. The heavy lines 
representing the Eustachian canals indicate their general direction in 



Fig. 99. —Skull of infant at term. Line A = level of nasal floor; line B = level of tympanic floor 



Fig. 100. —Skull of adult. Line A =level of nasal floor; line B =level of tympanic floor. 

relation to the horizontal plane,— i.e., they represent merely straight lines 
passing through the pharyngeal and tympanic orifices of the tube. The 
line A in each figure represents the level of the nasal floor, and the line B 




















TUBAL CATARRH LIST CHILDREN 


155 


the level of the tympanic floor. It is clear that the canal of the infant at term 
presents the following differences from the Eustachian tube of the adult: 

(1) It is shorter (14 mm.) and horizontal in direction, whereas the 
adult tube is 33 to 38 mm. long, and passes obliquely upward and back¬ 
ward to reach the tympanum at a considerably higher level. 

(2) The tympanic floor in the infant is on a level slightly below that 
of the nasal floor, while in the adult it is some 20 or 22 mm. above the 
floor of the nose. 

(3) The pharyngeal mouth of the infant canal is on about the same 
level as the hard palate, whereas in the adult it is some 10 mm. above the 
hard palate. 

To epitomize: The Eustachian tube of the infant is a short, relatively 
wide, horizontal canal, the pharyngeal orifice of which lies a little behind the 
choame and on a level slightly below that of the hard palate. Its phys¬ 
ical characteristics seem, therefore, as compared with the adult tube, partic¬ 
ularly favorable to the entrance of germs from the nasal secretion draining 
posteriorly into the pharynx, and to the development of vascular changes 
as a result of any pathological condition within the nose or nasopharynx. 

Absence of Subjective Symptoms. —One reason why tubal catarrh 
in children is not oftener diagnosticated as such is the absence of such 
symptoms as a young child would be able to describe, or likely to complain 
of. Children of a certain age complain promptly of pain, but such indefi¬ 
nite symptoms as a sensation of fulness in the ears they probably soon grow 
tolerant of. We begin life with hearing power so far in excess of our actual 
need that a child’s ears may be very seriously diseased before his hearing 
power becomes noticeably impaired. It is clear, therefore, that, if we are to 
recognize tubal catarrh in children at the stage at which it is most amen¬ 
able to treatment, we must make our diagnosis chiefly by the physical signs. 

Physical Examination. —I have already stated my belief that tubal 
catarrh is almost invariably present in children suffering from pharyngeal 
adenoids. Inspection of the ears of children in whom a physical exami¬ 
nation has demonstrated the presence of adenoids will, therefore, usually 
show the drum membranes to be markedly retracted. When the adenoid 
growth is of such size as to interfere seriously with nasal respiration, the 
drum membranes are usually retracted to a degree rarely seen in adults. 
They may also be noticeably congested. Beyond this there may be little 
to attract attention to the fact that the Eustachian canals are diseased or 
are not properly performing their function. 

Treatment.— The treatment is particularly important from the fact 
that the disease, if unchecked, probably represents the starting-point of 
morbid processes leading to deafness later in life. The indications are 
clear,— v i z>> removal of the pharyngeal growth, especial care being ob¬ 
served to avoid injury to the cartilage at the mouth of the tube, and 
subsequent treatment of the tubal lesion. For inflation of the ears we are 
usually obliged to resort to the Politzer method, few children being tol¬ 
erant of catheter inflation. Aside from the method of inflation, the treat¬ 
ment is practically the same as for adult patients. 


156 ACUTE DISEASES OF MIDDLE EAR AND MASTOID 


MYRINGITIS. 

Acute circumscribed inflammations limited to the drum membrane 
have been described by Politzer, Schwartze, and other distinguished ob¬ 
servers under the name of acute myringitis. Bezold, 4 on the other hand, 
felt so doubtful as to the propriety of separating such a lesion from a 
possibly coexisting inflammation of the middle ear, that he declined to 
recognize acute myringitis as a pathological entity. My own observations 
rather confirm the latter view, or at least convince me that the lesion is one 
of the rarest of aural diseases. I have seen, of course, innumerable cases 
in which the physical signs of inflammation were apparently confined to 
the drum membrane, but exceedingly few in which I was convinced that 
the middle ear was not also involved. I shall content myself, therefore, 
with a brief statement of the symptoms as described by others. 

The condition is said to have been observed with comparative fre¬ 
quency in association with influenza. It may be ushered in by a feeling 
of fulness and discomfort in the ear. This usually gives way to lancinating 
ear pain of moderate severity. In some cases the earache is of very severe 
type. With the pain, loud subjective noises often add to the patient’s 
distress. The hearing is usually only slightly impaired,—so little as often 
to escape the patient’s attention. In the early stage inspection of the drum¬ 
head may show marked injection of the membrana tensa, which is often 
particularly pronounced in the region of the hammer handle. Later, 
with exaggeration of the above changes, one or more bullae are seen, usually 
upon the posterior segment of the membrane. There may be also small 
ecchymoses, usually located in the posterior segment. The bullae, or blebs, 
may rupture into the external auditory canal. The course of the affection 
is usually short, ending in recovery. 

The disease is differentiated from acute otitis media by (a) the apparent 
limitation of the inflammatory changes to the external layers of the drum 
membrane, (b) the absence of bulging of the membrana tensa as a whole, 
and (c) the very slight impairment of hearing as compared with that 
usually accompanying acute middle-ear inflammation. 

The treatment naturally varies with the severity of the attack. The 
milder cases probably recover with little or no treatment. Moderate 
pain may be relieved by the application of dry heat,— i.e., lying with the 
affected ear resting upon a hot-water bag. In cases in which the earache 
is unbearably severe, the author believes that by far the safest method of 
obtaining relief is that employed in acute otitis media,—viz., free incision 
of the drum membrane and subsequent cleansing of the canal by means 
which will be described in connection with the treatment of acute tympanic 
disease. This plan of treatment gives prompt relief of pain and at the 
same time insures against the retention of inflammatory products which 
may collect within the tympanum. 

-Bezold: Text-book of Otology, p. 123. 


r 






ACUTE MIDDLE-EAR INFLAMMATION 


157 


ACUTE MIDDLE-EAR INFLAMMATION. 


Nomenclature: Significance of Names in Common Use. Before 
discussing separately the acute tympanic lesions, we should endeavor to 
define as clearly as may be just what we intend to convey as to the charac¬ 
ter of the lesions by the common terms “acute catarrhal otitis media’ 7 
and “acute purulent otitis media.” If the question were considered solely 
from a bacteriological viewpoint, it would be clearly possible to obtain in 
every case a specimen of the tympanic secretion, and according to the 
absence or presence of bacteria to say that we have to deal with either a 
serous or a purulent otitis media. It is neither possible nor desirable, 
however, in actual practice to base one’s diagnosis wholly upon the bac¬ 
teriological findings, and there are obvious advantages in the adoption 
of a simple classification which may be based upon such data as one may 

obtain from a careful examination of the patient. 

According to the investigations of Zaufal and many who have followed 
his line-of work, there are reasonable grounds for questioning whether 
acute inflammatory processes ever involve the middle-ear cavity in the 
absence of pathogenic bacteria. He found in a large series of examinations 
that pus germs were always present in the tympanic secretion taken from 
acutely inflamed ears; and, per contra, that no cultures could be obtained 
from secretions taken from apparently normal ears. Accepting this theory 
as generally correct, we must yet admit that certain congestive conditions 
_ e tubotympanic congestion with effusion of serum may be accom¬ 
panied by distention and vascular engorgement so pronounced as to repro¬ 
duce all the clinical and physical phenomena of acute purulent otitis 
media and to constitute a condition not clinically distinguishable there- 


Bezold, in discussing the nomenclature of tympanic disease, objected 
to the use of the word “catarrhal” as applied to middle-ear inflammations. 
He based his objection largely upon certain histological features of the 
lining membrane of the tympanum which seemed characteristic of a serous, 
rather than of a mucous, membrane. Thus, while the mucous membrane 
of the cartilaginous portion of the Eustachian tube is thick, lined by sev¬ 
eral layers of ciliated epithelium, and contains many acinous glands, the 
lining membrane of the tympanum is exceedingly thin, contains no acinous 
glands, and is devoid of cilia except upon the floor. In the atrium it con¬ 
sists for the most part of a single layer of basement cells very closely 
adherent to the periosteum, and has a decidedly endothelial character. The 
mucous membrane of the pharyngeal half of the Eustachian canal secretes 
more or less rather thick mucus, whereas the normal secretion of the tym¬ 
panum is very thin and serous in character. Bezold, therefore, proposed 
to omit the term “catarrhal” from descriptions of tympanic inflammation, 
and to substitute the word “simplex/’-thus “otitis media simplex acute 
as differentiated from “otitis media catarrhahs acuta. The word sim¬ 
plex,” thus used, is in no way descriptive, however, and is open to the 


158 ACUTE DISEASES OF MIDDLE EAR AND MASTOID 


further objection that it would prove in many cases actually incorrect or 
misleading, since it is often impossible to determine clinically whether an 
acute tympanic lesion is or is not purulent in character. It would seem 
better, therefore, not to discard old, time-honored names, which have 
obtained such widespread adoption, but rather to define clearly the charac¬ 
ter of the lesion they are intended to describe. 

There are three common forms of acute middle-ear inflammation, an 
appreciation of which helps to a clearer understanding of the varying 
phases of tympanic disease,—viz. (1) An acute serous otitis media ,— i.e. 
a non-purulent inflammation with effusion of serum into the cavity of the 
atrium; (2) an acute purulent inflammation confined to the atrium; and (3) 
an acute purulent inflammation involving both the atrium and the tympanic 
vault. It may be quite impossible, however, by its clinical manifestations 
to distinguish an acute serous, or non-purulent, otitis media from an acute 
purulent otitis media. In either the membrana tensa may be red and 
bulging, the subjective symptoms are often identical, and the indications 
for treatment are practically the same. From the standpoint of practical 
otology, therefore, it seems best to consider acute middle-ear inflammation 
under two heads,—viz. (1) u Acute catarrhal otitis media,'’ by which term 
we shall designate any acute inflammation, purulent or non-purulent, 
confined to the atrium; and (2) u acute purulent otitis media,” or an acute 
inflammation involving both the atrium and the tympanic vault. These 
two conditions undoubtedly represent respectively the simpler and the 
more serious forms of acute tympanic disease as met with in actual practice. 

Otitis Media Catarrhalis Acuta; Acute Catarrhal Otitis Media.— 
These terms we apply to the simpler form of acute middle-ear inflammation, 
— i.e., an acute inflammatory process confined to the atrium. 

Etiology. —The causes have already been enumerated in a fore¬ 
going chapter. Depressed constitutional states, and therefore exhausting 
diseases, render the individual more prone to tympanic disease. Obstruc¬ 
tive lesions of the nose or nasopharynx— i.e., conditions interfering with 
nasal respiration—are strongly predisposing factors. Pharyngeal adenoids 
react injuriously upon the ears, and are responsible in large measure for 
the prevalence of tympanic disease among children. 

Exciting Causes. —Gauging their importance as proportional to the 
number of cases to which they give rise, the exciting causes should be 
mentioned in the following order: (1) Acute nasopharyngitis, — i.e., the 
common “cold in the head.” More cases of acute middle-ear inflammation 
can be accounted for as secondary to this affection than can be traced to 
any other cause. (2) The acute exanthemata: scarlet fever, diphtheria, 
and measles cause acute tympanic disease with even greater frequency 
than is generally recognized by the medical profession. Scarlet fever is 
accompanied by acute tympanic disease more frequently than is diph¬ 
theria, and the proportion of scarlatinal cases which go on to acute sup¬ 
purative mastoiditis is considerably larger. Measles is a very frequent 
cause of acute otitis media of rather severe type in which mastoid suppura- 


OTITIS MEDIA CATAERHALIS ACUTA 


159 


tion occurs with marked frequency. Acute epidemic influenza gives rise 
to acute otitis media, often of very severe type. The proportion of cases 
in which this complication occurs varies in different epidemics according 
to variations in the average severity of the disease. (3) The nasal douche: 
it is a recognized fact that many cases of acute middle-ear inflammation 
are caused by the careless use of the nasal douche in cases of atrophic 
rhinitis, ozsena, etc. In the milder cases of nasopharyngeal disease, the nasal 
spray will be found an efficient, and certainly safer, method of cleansing 
the nose. (4) Diving or swimming under water: the frequency of tympanic 
inflammation from this cause is evidenced by the large number of patients 
presenting themselves each year at the beginning of the swimming season. 
The injury to the ears may occur in one of two ways,—viz. (a) by expulsion 
of water taken into the nose or throat through the Eustachian tubes or 
(b) by impact of the cold water against the drum membrane. The latter 
danger may be practically eliminated by stopping each auditory canal 
with a pleget of moistened absorbent cotton. (5) Traumatic injuries of 
the drum membrane are a comparatively rare cause of acute middle-ear 
inflammation. Of such injuries the commonest is that caused by a for¬ 
cible box or slap upon the ear, the drum membrane being ruptured by the 
sudden condensation of the air in the external auditory meatus. 

Micro-organisms found in the Ear during Acute Middle-ear Inflammation. 
—A very large number of micro-organisms have been found in the secre¬ 
tions taken from the ear during acute otitis media, those most frequently 
found are the streptococcus, the pneumococcus, and the streptococcus 
mucosus. Next in frequency are the staphylococcus albus and staphylo¬ 
coccus aureus, and after these come the bacillus proteus, the bacillus 
pyocyaneus, and a long list of organisms which do not call for special 
mention here. 

As regards the comparative virulence of these germs in relation to 
aural disease, there is no longer room for doubt that the streptococcus and 
pneumococcus give rise to a type of middle-ear suppuration which leads 
more frequently to intracranial infection than do the tympanic lesions 
caused by the staphylococci or other germs mentioned. Suepfle, from an 
analysis of the bacteriological findings in a large series of cases, concluded 
that cases of acute otitis media due to staphylococcus infection do not 
give rise to intracranial complications. M hile this view is extreme, and 
therefore incorrect, it serves to emphasize the infrequency of intracranial 
disease secondary to staphylococcus infection. The streptococcus, on 
the other hand, is unquestionably responsible for a majority of cases of 
intracranial disease of otitic origin. 

Accepting the above statements as in the main conect, one must ^ et 
acknowledge that one can not prognosticate from the micro-organism 
found in the tympanic discharge the future course or severity of the aural 
disease, this being determined quite as much by the patient’s systemic 
condition,— i.e., the question of normal or lowered resistance. A staphy¬ 
lococcus may, therefore, produce clinically an exceedingly severe type of 


160 ACUTE DISEASES OF MIDDLE EAR AND MASTOID 


inflammation; whereas a mild type of acute otitis media may result from 
a streptococcic invasion of the ear. 

Anatomical Conditions in Relation to Symptoms. It may be 
well, before discussing clinical phenomena, to review briefly certain ana¬ 
tomical features of the atrium which bear rather directly upon the symp¬ 
toms and course of the simpler form of acute otitis media. 

It will be recalled that the cavity of the atrium is lined by an exceedingly 
thin membrane very closely adherent to its walls. Externally the atrium is 
closed by the tense, inelastic and rather unyielding membrana tensa. 
Superiorly the atrium is more or less completely separated from the tym¬ 
panic vault by the structures massed in this situation,—viz., the neck and 
short process of the malleus; the lower anterior extension of the body of 
the incus; the anterior, external, and posterior ligaments of the malleus, 
and the mucous membrane which surrounds them. From the anterior 
wall of the atrium the Eustachian canal leads forward, inward, and down¬ 
ward into the nasopharynx. Germs reaching the tympanum from the 
nasopharynx by way of the Eustachian tube lodge first, therefore, in the 
atrium. 

An inflammatory process originating in and confined to the atrium 
probably represents changes taking place somewhat in the following 
order: (1) Marked dilatation and engorgement of the vessels of the lining 
membrane; (2) transudation of serum and migration of leucocytes from 
the veins into the tissues of the mucoperiosteal lining. The consequent in¬ 
flammatory thickening of the lining membrane has the important mechani¬ 
cal effect of rendering the separation of the atrium from the vault more 
complete. The bony Eustachian tube is also more or less closed by inflam¬ 
matory swelling in the region of the tympanic orifice. With the formation 
of pus or effusion of serum into the atrium, the walls of that cavity are, 
therefore, soon subjected to pressure, the outer wall, or membrana tensa, 
being the one which offers least effective resistance. Hence the early 
spontaneous rupture of the drum membrane—usually in six to twenty- 
four hours—which commonly occurs in acute catarrhal otitis media. 

As compared with the vault, the relatively small amount of connective 
tissue in the atrium (consisting chiefly of its thin and closely adherent 
lining membrane) constitutes another condition favorably influencing the 
progress of the disease. That is to say, the fastigium being passed, the 
tissues more quickly regain an approximately normal condition, the 
patency of the Eustachian tube being restored, and the mechanical con¬ 
ditions favorable to resolution being more quickly established. 

Symptoms and Signs. —When acute otitis media occurs as a compli¬ 
cation of one of the acute infectious diseases, the otitic symptoms may for 
a time be more or less masked by those of the initial disease. When, on 
the other hand, the aural disease is not secondary to a systemic infection, 
the onset is usually sudden and clearly defined. 

As a prodromal symptom, a sensation of fulness or occlusion of the 
ear is noted by some authors as of frequent occurrence. This symptom, 


OTITIS MEDIA CATARRHALIS ACUTA 


161 


when present, is clearly a result of the tubal catarrh, or congestion, which 
almost invariably precedes or accompanies acute catarrhal otitis media. 
According to the writer’s observation, the symptom first experienced, or 
at least first complained of, by the patient is usually pain. 

Onset .—The earache is usually sudden in its development. Following 
a few premonitory twinges, it soon assumes the character of a constant 
pain, rapidly reaching an unbearable degree of severity. Not infrequently 
the patient retires at night with no noticeable discomfort, to be awakened 
during the night or toward morning by the severity of the ear pain. Once 
established, the pain is usually constant, but is subject to exacerbations 
of intensity. With the beginning of pus formation, the pain becomes 
throbbing or “drawing” in character, being sometimes compared by the 
sufferer to the severe form of toothache usually accompanying an abscess 
at the root of a carious tooth. Naturally, sleep becomes impossible; and 
when prompt relief is not forthcoming, the resulting insomnia adds to the 
nervous strain to which the patient is subjected. The severity of the pain 
often distracts the patient’s attention from lesser symptoms. If ques¬ 
tioned, however, he usually becomes conscious of subjective sounds, 
i.e., tinnitus aurium. The hearing is also noticeably impaired, showing 
certain characteristic changes which will be referred to later. 

The constitutional symptoms vary widely with the age, and also to 
some extent with the nervous constitution of the patient. With adults, 
the temperature may throughout be normal or nearly so, or it may be 
moderately elevated. With infants and young children, on the other 
hand, even the mildest type of acute middle-ear inflammation is usually 
announced by rather high fever,— i.e., temperature ranging from 102° to 
105° F. The temperature variations which both adults and children occa¬ 
sionally exhibit with mild grades of tympanic inflammation depend probably 
upon individual differences in the stability of central nervous control. 
That is to say, it seems necessary in some cases to refer the fever to a reflex 
disturbance of the cerebral heat centres, rather than to the influence of 
septic absorption from the ear. Certainly the rapid and considerable 
elevations of temperature frequently seen in children suffering from the 
simplest type of acute tympanic inflammation are in many cases most 
easily explained in accordance with the above hypothesis, i.e., as a reflex 

phenomenon. , 

With patients of all ages, adults as well as children, digestive disturb¬ 
ances are common during the early stages of an acute catarrhal otitis 

media. . , ,, 

Spontaneous Rupture of the Drum Membrane— As we have seen, the 

atrium during acute catarrhal otitis is a small, closed cavity, the outer, 
membranous wall of which represents the direction of least, resistance. 
Obviously the membrana tensa must give way before any rapid accumu a- 
tion of pus or serum. Spontaneous rupture of the drum-head usually 
occurs within six to twenty-four hours after the onset,—or, to be more 
exact, after the appearance of the initial earache. 

11 


162 ACUTE DISEASES OF MIDDLE EAB AND MASTOID 

With the rupture of the drum membrane and the appearance of aural 
discharge, there is usually complete cessation of pain. The adult patient 
usually experiences an immediate sense of relief, and the child, which as 
been tossing about the bed in distress, now falls into a sleep of exhaustion. 
The temperature, which in young children is usually elevated, may fall 

within a few hours to the normal line. 

With adult patients, two symptoms, probably in some degree present 
from the onset, are now thrown into bolder relief, and become the patient s 
chief cause of concern,—viz., tinnitus aurium and impairment of hearing. 

Tinnitus Aurium .—The subjective sounds apparently vary greatly in 
different individuals. On the other hand, it may be that the variations 
are often more apparent than real, depending upon the natural difficulties 
in describing a purely subjective sensation. Thus, we aie frequently told 
that the noise is like the “noise of a tea-kettle/’ “the escaping of steam,” 
“whistling of wind in the trees,” “the sound of a cricket,”—all which 
comparisons may be intended to describe the same charactei of sound. 
Again the sound is compared to a ringing of bells or to a shrill whistle, 
i.e., sounds of different character. From the average statements of intel¬ 
ligent patients, one is led to believe that the sound is usually of rather 
high pitch. 

Tinnitus which has made its appearance during, and as a result of, an 
attack of acute otitis media usually disappears when the last physical 
evidence of inflammation has gone. It is, however, in my experience 
often the very last symptom to disappear. 

Impairment of Hearing .—The hearing is always impaired at the height 
of an acute catarrhal otitis media. At the onset,— i.e., during the stage 
preceding the accumulation of fluid in the tympanic cavity—the impair¬ 
ment may be slight, or not noticeable. As serum or pus displaces the air 
in the tympanum, however, the hearing power is usually considerably 
reduced. 

The type of impairment assumes to some extent the general character 
of deafness due to disease in any part of the conducting apparatus,— i.e., 
hearing by bone conduction is increased, and the ratio between hearing by 
bone conduction and by air conduction is changed, though not necessa¬ 
rily reversed. 

Bezold called attention to certain features of the disturbance of hearing 
as characteristic of acute middle-ear inflammation with effusion. In acute 
otitis media with bulging of the drum membrane, bone conduction is 
increased, and the tuning-fork held in contact with the mid-line of the 
skull is referred definitely to the diseased organ. With this increase in 
bone conduction there is, however, according to Bezold, surprisingly little 
disturbance of audition for the low musical tones, some of his patients 
hearing tones as low as 16 d.v. This is the reverse of what one usually 
finds in chronic lesions of the conducting mechanism, in which the lower 
tone limit is almost invariably considerably elevated. Bezold explains 
this difference by reference to differences in the pathology of the two types 


OTITIS MEDIA CATARRHALIS ACUTA 


1G3 



Fig. 101. 


of disease. Thus, in chronic middle-ear disease, either suppurative or 
non-suppurative, there is usually present either partial destruction of the 
drum membrane, or fixation of the membrane or ossicles. Either of these 
conditions would interfere markedly with the slow and extensive movements 
involved in the production of very low musical tones. In acute catarrhal 
otitis media, on the other hand, disturbance of function is due largely to 
the presence within the tympanum of fluid which 
acts as a weight upon the drum membrane and 
ossicles, interfering with the acuteness of hearing 
for all sounds, but not necessarily offering special 
resistance to the slow and relatively wide vibrations 
necessary to the transmission of the lower tones 
of the musical scale. 

Obviously, the presence of fluid in the tym¬ 
panum is not the only factor in the deafness of 
acute otitis media, the other being the inflam¬ 
matory infiltration of the drum membrane and 
tympanic mucosa. This explains the fact that 
some degree of deafness often considerably outlasts 
the cessation of the discharge and final closure 
of the drum membrane. 

Physical Changes in the Drum Membrane .—The 
physical appearance of the drum membrane varies 
materially with the time which has elapsed since the 
onset. If seen very shortly after the earache is first 
experienced, the drum-head will be found deeply 
injected,— i.e., exceedingly red. When different 
portions of the tense membrane show variations in 
this respect, the upper part is usually more deeply 
injected than the lower portion, which may be 
nearly or quite normal in color. In other words, 
the injection is said to appear first above and extend 
downward; but there is never any line of demarca¬ 
tion between the injected and normal portions, 
the one shading gradually into the other. In a 
majority of cases, however, the whole membrana 
tensa when first seen by the physician is uni¬ 
formly red (Fig. 101). 

If the examination be delayed a few hours, 
inspection of the drum membrane may reveal 



Fig. 103. 

Figs. 101, 102, and 103- 
Acute catarrhal otitis media. 
1st, 2d, and 3d stages. 


an entirely different 


picture,—'i.e., the membrana tensa is now not only exceedingly red, but 
bulges markedly outward into the lumen of the meatus. A slight central 
depression may be seen in the position of the umbo. Other than this, 
the normal landmarks, including the short process and handle of the 
malleus, may be more or less obliterated or hidden from view (Fig. 102). 

If the examination be still further delayed, we shall be likely to find tne 








164 ACUTE DISEASES OF MIDDLE EAR AND MASTOID 


canal filled with pus, in which case we can, of course, see nothing of the 
drum membrane until the ear has been irrigated or the meatus otherwise 
cleansed. It is then possible to locate the perforation, which is situated 
practically always in the posterior segment of the membrane. Most 
frequently it is found in the posterosuperior quadrant,— i.e., behind the 
hammer handle. Occasionally a perforation is so minute that one is not 
quite sure of its recognition. In such a case, if the patient is required to 
perform Valsalva inflation while the drum membrane is kept in view, a drop 
of pus will be seen to exude, thus locating definitely the site of the per¬ 
foration (Fig. 103). 

The Discharge .—Following rupture or incision of the membrane, the 
discharge may vary considerably, in accordance with certain conditions, 
— e.g., the constitutional condition of the patient, the character of the in¬ 
fection, the time elapsing between the onset of the disease and the rupture 
of the drum membrane, and, of course, with the efficiency of the treatment. 
If the inflammation is serous, or non-purulent, and the rupture of the drum¬ 
head has occurred early, the discharge may remain serous in character and 
last but a few days. If, on the other hand, the patient is in a constitu¬ 
tionally exhausted condition, or the infection is of virulent type, and par¬ 
ticularly if the rupture of the drum membrane has been considerably 
delayed, the discharge is likely to be more profuse and to persist longer. 

Taking as an example a case in which an intensely red and bulging 
drum membrane has been properly incised, the discharge may pursue some¬ 
what the following course: Frequently it does not reach its maximum 
flow during the first twelve or twenty-four hours following the incision. 
The writer has repeatedly been impressed with the relatively moderate 
discharge immediately following myringotomy in cases of severe tympanic 
inflammation. After the first twelve or twenty-four hours it rapidly 
increases in amount, usually reaching the maximum on the second or third 
day. From this point it may for a few days be exceedingly profuse, then 
gradually receding. Its disappearance may be quite rapid, or, for no reason 
discernible in the physical character of the lesion or the type of infection, 
be comparatively slow. Finally, after the amount is reduced to an apparent 
minimum, it may persist obstinately for days, suddenly ceasing with the 
complete closure of the drum membrane. Following the closure of the 
incision, the drum membrane may rapidly regain its normal appearance 
or weeks may elapse before all traces of the recent inflammatory process 
have disappeared. 

The above describes somewhat in detail the usual course of an attack 
of acute catarrhal otitis media. The whole process, from the appearance 
of the discharge to final closure of the drum membrane, may run its course 
in a week or less, or may be spread over two or three weeks or more. To 
understand these otherwise puzzling variations, we must recognize in the 
patient’s general power of resistance, or departure from the normal 
therein, a factor quite as potent in deciding the course of the disease as the 
character of the infection itself. 


OTITIS MEDIA PURULENTA ACUTA 


165 


In the writer’s opinion, serious complications of acute catarrhal otitis 
media rarely occur without previous change in the character of the lesion,— 
i.e., without extension of the infection to the structures of the vault. 

The prognosis as to ultimate recovery is good. The drum membrane 
usually heals without noticeable cicatrices or structural changes. Per¬ 
manent impairment of hearing is exceedingly rare. There can be no doubt 
that a mild attack in which final healing is unduly delayed is more apt to 
result in some permanent impairment of function than a severe lesion in 
which prompt local recovery occurs. On the other hand, a very prolonged 
attack may leave absolutely perfect hearing. 

Acute Suppurative Otitis Media; Acute Purulent Otitis Media 
(Otitis Media Purulenta Acuta).— These terms are employed to describe 
a suppurative inflammation involving both atrium and vault. In many 
cases the inflammatory process seems to originate in the vault, spreading 
thence downward to the atrium; in others, an infection of the atrium extends 
upward to the attic. 

Etiology. —The causes of acute purulent otitis media are the same as 
those giving rise to the simpler form of acute tympanic inflammation. 
They do not, therefore, call for repetition here. So also of the bacteriology, 
—there is no organism which may cause one grade of acute middle-ear 
inflammation and not the other. That is to say, the same exciting cause, 
or the same pathogenic micro-organism, may give rise either to the simpler 
or the more severe form of otitis media, this depending perhaps to some 
extent upon variations in the individual s vitality or resistance power to 

disease. 5 

Anatomical Conditions Influencing the Pathology of the 
Disease. —The anatomico-surgical features of the vault are perhaps best 
shown by comparing them with those of the atrium. It will be remem¬ 
bered that the atrium contains but little connective tissue other than the 
thin and closely adherent membrane lining its walls. Inflammation tends, 
therefore, to be self-limited, by reason of the very limited field involved, 
and the rather unfavorable nidus provided for the growth of germs, d he 
mechanical separation of the atrium from the vault is rendered more 
complete by the inflammatory swelling of mucosa, this favoring early rup¬ 
ture of the drum-head, with consequent drainage and relief of tension, 
i.e., early resolution. As congestion about the Eustachian orifice subsides, 
the Eustachian canal provides a supplementary drain for the escape of 


serum or pus. 


5 The frequent occurrence of suppurative lesions, apparently originating in the vault, 
is rather difficult to explain. Why should germs presumably entering by way of the 
Eustachian canal primarily infect the vault? In trying to account for this phenomenon 
the following theory has seemed to the writer the most satisfactory,—viz., that the 
atrium presents certain conditions unfavorable to the development of Purulent inflam¬ 
mation which do not exist in the vault; that germs entering by way of the Eustachian 
canal may pass through the atrium without infecting its mucosa, and, reaching the vault 
may find there the conditions favorable for the inception and spread of a suppurative 

inflammation. 





166 ACUTE DISEASES OF MIDDLE EAR AND MASTOID 


The vault (Fig. 104) presents the following features bearing upon the 
pathology of suppurative lesions originating therein: (a) It is directly 
continuous posteriorly with the so-called mastoid antrum. Pus collecting 
from a primary infection in the Vault is not, therefore, quickly subjected 
to pressure,—flowing rather backward along the pathway of least resist¬ 
ance into the antrum. The antrum is early involved in acute 'purulent otitis 
media , and from the onset the danger of suppurative mastoiditis is greater. 
The escape of pus downward into the atrium frequently represents a later 
stage,— i.e ., is subsequent to the accumulating of pus within the antrum. 
Spontaneous rupture of the drum membrane is often therefore delayed, 
usually from forty-eight hours to a week, (b) There is no natural path- 



Malleo-incudal fold 
depending from tym¬ 
panic roof and cover¬ 
ing upper surfaces of 
malleus and incus 


Artificial opening in 
malleo-incudal fold, 
leading into inner 
chamber of vault 

Antrum 


Horizontal membranous fold, 
dividing outer chamber of vault 
into an upper and lower space 


Fig. 104. —Diagrammatic picture of membranous partitions of vault. 


way providing for the free escape of pus from the vault, and even extensive 
incision of the drum membrane does not provide free and adequate drain¬ 
age from the antrum, (c) The lining membrane of the vault is not closely 
adherent as in the atrium, but hangs in folds from the tympanic roof, 
covering the head of the malleus and body of the incus, and dividing the 
attic into an outer and inner compartment. Another fold of mucous 
membrane is usually present, passing horizontally across the outer cham¬ 
ber of the vault, and dividing it further into an upper and lower space. 
This surplus of vascular connective tissue forms a suitable nidus for the 
growth of infective germs, and favors the development of suppurative 
inflammation. The subdivision of the vault cavity into membranous 
compartments is also distinctly favorable to the retention of pus, and 
therefore to the spread of infection. 

Symptoms and Signs. —The subjective symptoms of acute suppurative 
otitis media do not differ greatly from those of the simpler form. Earache 
is usually the first purely aural symptom of which the patient complains. 




OTITIS MEDIA PURULENTA ACUTA 


167 


The ear pain resulting from a primary infection of the vault is, perhaps, a 
little less sudden in its attack, and somewhat slower in reaching its max¬ 
imum intensity, than that accompanying a similar lesion confined to the 
atrium. It is also much less likely to be relieved by early rupture of the 
drum membrane. It is described as a most unbearable type of pain, 
throbbing or boring in character,—and soon reaching a degree of severity 
rendering sleep impossible. From the onset, the patient usually experiences 
subjective noises,—this symptom, however, being over-balanced by the 
severity of the pain, and therefore rarely complained of at this stage of 
the disease. The hearing may at first be but little disturbed, this depend¬ 
ing upon the extension of the inflammation to the membrana tensa and 
structures about the oval window and incudostapedial joint, and upon 
the accumulation of pus within the atrium. As the lesion advances, the 

hearing is always markedly impaired. 

Some degree of fever is usually present in the acute stage. With adults 
the temperature may rise to 102° F. or more, or may be but slightly above 
the normal. With infants and young children, on the other hand, rather 
high temperature is the rule. Owing partly to the fever, when present, 
but chiefly to the severity of the pain and the consequent insomnia, there 
are few circumscribed lesions which will more quickly exhaust the patient 
than an attack of acute middle-ear inflammation which has not been re¬ 
lieved by rupture or incision of the drum membrane. 

Spontaneous Rupture of the Drum Membrane. The interval between the 
initial pain and the rupture of the membrane is usually much longer than in 
the simpler form of acute otitis media. In my experience, it varies all the 
way from forty-eight hours to a week. This wide variation is probably 
explained by differences in the early pathways of extension. If, for example, 
a suppurative process in the vault extends quickly in the direction of the 
atrium, or is quickly followed by a secondary infection of the lower tym¬ 
panic space, pus collecting there will be likely to cause a compai atively ear Iv 
rupture of the membrane. On the other hand, a primary infection of the 
vault, spreading chiefly backward in the direction of the antrum, may tor¬ 
ture the patient for days before pus, accumulating in the atrium, causes 
rupture of the membrana tensa. Such cases are best studied in dispensary 
practice, where patients frequently come under observation who have suf¬ 
fered three, five, or even six days without rupture of the membrane. 
It is not difficult to appreciate why final rupture of the membrane in these 
cases often affords much less relief than that which almost invariably 
follows the early rupture of the drum-head in acute catarrhal otitis media. 

Physical Signs .—It is clear that the physical changes in the drum 
membrane must vary with the progress of the disease. We shall try, 
therefore, to describe certain conditions, representing progressive stages 
of the lesion, in the order in which they would be likely to occur. 

If the patient is seen very shortly after the initial symptom, we may 

find the following conditions present: 

1. The membrana tensa throughout the greater part of its extent may 


168 ACUTE DISEASES OF MIDDLE EAR AND MASTOID 



Fig. 105. 



Fig. 106. 


be quite normal in color and appearance. The upper posterior portion of 
the tense membrane,—that part immediately contiguous to Shrapnell 8 

membrane,—and ShrapnelPs membrane itself, are 
intensely red, and, if not actually bulging, have 
the appearance of acute inflammatory infiltration 
(Fig. 105). This condition is very frequently 
observed in patients who are seen just after the 
onset, and usually indicates a suppurative process 
in the vault, which later will extend downward 
and involve the atrium. 

2. A few hours or one or two days later, we 
may see the following changes: the upper half or 
whole of the membrana tensa is red, or injected. 
The injection in the region of ShrapnelPs mem¬ 
brane is, however, much more intense, and the 
inflammatory thickening (infiltration) in this region 
is so pronounced as to indicate clearly a suppura¬ 
tive process behind ShrapnelPs membrane,— i.e., 
in the vault (Fig. 106). This picture is often seen 
in acute suppurative inflammation of the attic, and 
occurs at a period following the onset which in a 
similar lesion of the atrium would have been 
marked by noticeable bulging or rupture of the 
drum membrane (Figs. 102 and 103). 

3. The upper posterior part of the membrana 
tympani— i.e., the part including and immediately 
adjacent to ShrapnelPs membrane—is markedly 
bulging, clearly indicating the presence of pus in the 
tympanic vault (Fig. 107). With this condition, the 
entire membrana tensa also is invariably inflamed. 
The bulging, however, is confined to, or most con¬ 
spicuous in, the region of ShrapnelPs membrane. 

4. The canal contains pus, removal of which 
reveals the following conditions,—viz., entire drum 
membrane (membrana tensa and membrana flac- 
cida) red and bulging. Small perforation in pos¬ 
terior segment of membrana tensa. Posterosuperior 
canal wall— i.e., that part immediately adjoining 
the drum membrane — is frequently very con¬ 
siderably swollen, so that no line of demarcation 
is here discernible between canal wall and drum 
membrane (Fig. 108). This condition always 
indicates a severe suppurative process within the 
vault, and frequently coexists with inflammation 

It is commonly spoken of as “sagging of the 



Fig. 108. 

Figs. 105,106,107, and 108. 
—Acute purulent otitis 
media, 4 successive stages. 


of the mastoid cells, 
posterosuperior canal wall.” 
















ACUTE OTITIS MEDIA IN INFANTS 


169 


Antrum Tenderness .—It must be clear, from a study of tympanic 
anatomy (Fig. 104), that pus collecting in the tympanic vault must soon 
find its way into the antrum. The antrum, therefore, is usually to some 
extent involved in a suppurative inflammation of the vault, and sensitive¬ 
ness to pressure over the antrum is rarely altogether absent from the 
most acute stage of an acute purulent otitis media. 

Course of the Disease .—The course of an uncomplicated case of acute 
suppurative otitis media is somewhat similar to that of the acute “catar¬ 
rhal” form, but is usually more prolonged. Some very severe cases, how¬ 
ever, make surprisingly rapid recoveries. The discharge—increasing dur¬ 
ing the first day or two following myringotomy—is usually very profuse 
at first, its duration depending upon the patient’s constitutional condi¬ 
tion, the virulence of the infection, and the extent of the area involved 
in the vault and antrum. The best possible incision through the drum 
membrane may not provide perfect drainage of the membranous pockets 
of the vault, and can not adequately drain the antrum. The process of 
resolution includes, therefore, the removal of pus in part through an in¬ 
cision or perforation of the drum-head, and in part by its elimination 
through the lymphatic system. In. a favorable case, the discharge may 
cease and the drum membrane close in a period varying from ten days to 
four weeks. 

Acute Otitis Media in Infants .—Before leaving the discussion of symp¬ 
toms, a word should be said as to the diagnosis of acute middle-ear inflam¬ 
mation in infants and young children. 

It has been frequently stated in otological literature that acute otitis 
media in young children is invariably announced by a considerable eleva¬ 
tion of temperature. This is not strictly true. In the Willard Parker 
Hospital for Acute Infectious Diseases, the writer has seen a number of 
cases in which an acutely inflamed ear with bulging of the drum membrane 
has coexisted with a normal or but slightly elevated temperature. Such 
cases, however, form so small a percentage of the total number of cases in 
young children, that they are to be regarded, perhaps, as the exceptions 
which prove the rule. They are mentioned simply to emphasize the fact 
that one can not with certainty exclude acute tympanic disease even in 
young children by the absence of fever. As a general rule, however, it is 
perfectly correct to say that in the great majority of cases, even the milder 
grades of acute middle-ear inflammation give rise to a very considerable 
rise of temperature. 

In a child of three years or less, the subjective symptoms of acute otitis 
media are often so indefinite as to be of little or no diagnostic value to the 
general practitioner. So skilful and experienced an observer as Dr. C. G. 
Kerley 6 has stated his belief that young children do not, as a rule, experience 
earache with acute middle-ear inflammation. While I have never been 
able to accept this view as quite justifiable, it is certainly remarkable how 

g Kerley: Symptomatology of Acute Otitis in Children, New York Medical Journal, 
July 8, 1905. 






170 ACUTE DISEASES OF MIDDLE EAR AND MASTOID 


long a bright little child may suffer from an acute tympanic lesion with¬ 
out directing attention to the ear. If earache is not always an avail¬ 
able symptom, it is obvious that such subjective phenomena as tinnitus 
aurium and moderate impairment of hearing are often quite indeter¬ 
minable in young children. 

If I were called upon to enumerate the symptoms of acute tympanic 
disease in young children, I should give them in somewhat the following 
order: 

1. Fever: high temperature—102° to 105° F — is present in the great 
majority of cases. Unexplained temperature should, therefore, call for 
prompt examination of the ears. 

2. Earache , when complained of, is, of course, the most useful sub¬ 
jective symptom. 

3. Restlessness, shown by irritability of temper, peevishness, loss of 
interest in play, crying without apparent cause, sleeplessness at night, or 
restlessness (tossing) during sleep—one or any of these symptoms should, 
unless otherwise accounted for, be regarded as pointing to possible tym¬ 
panic disease. 

4. Grabbing at the ears, or rubbing the ears, during sleep or during the 
waking hours, is regarded as a sign of tympanic pain, and undoubtedly 
often helps to locate a tympanic lesion. It is often, however, a sign simply 
of restlessness from other causes, examination showing normal ears. It 
may, therefore, be a useful sign, but is by no means pathognomonic. 

Besides those above mentioned, there are of course an army of symp¬ 
toms which may be present during acute tympanic disease, but which can 
not be described as characteristic thereof. I believe very firmly that the 
routine practice of examining the ears of all sick children would prevent 
not only much unnecessary suffering, but also some loss of life. 

Complications of Acute Purulent Otitis Medta.— 

1. Acute suppurative mastoiditis: which may give rise to 

(a) Infective sinus thrombosis. 

(b) Epidural abscess. 

(c) Cerebral abscess. 

(d) Cerebellar abscess. 

(e) Acute diffuse suppurative labyrinthitis. 

(f) Acute circumscribed suppurative labyrinthitis. 

(g) Purulent leptomeningitis. 

2. Acute serous labyrinthitis. 

3. Acute diffuse suppurative labyrinthitis: which may lead to 

(a) Epidural abscess. 

(b) Cerebellar abscess. 

(c) Purulent leptomeningitis. 

(d) Infective sinus thrombosis. 

4. Direct infection of the jugular bulb (rare). 

The above are given in what I believe to be the order of their frequency. 
Some of the lesions included under acute mastoiditis might, theoretically, 


TREATMENT OF ACUTE OTITIS MEDIA 


171 


be included among the sequelae of acute purulent otitis media. They 
occur so rarely, however, without intermediate infection of either the 
mastoid process or the labyrinth, that the above scheme gives a much 
more correct view. 

Acute circumscribed suppurative labyrinthitis is included among the 
possible sequelae of acute mastoiditis, but not among those of acute puru¬ 
lent otitis media, because direct infection of the labyrinth from a tympanic 
lesion usually proceeds through one of the labyrinthine windows, and is 
almost invariably diffuse. Acute circumscribed suppurative labyrinthitis 
results most often from necrosis of one of the semicircular canals, the 
horizontal canal being the commonest point of attack. This practically 
never results directly from an acute tympanic lesion. Infection of the 
jugular bulb as a direct result of purulent otitis media— i.e., without inter¬ 
mediate infection of the mastoid cells—is a somewhat rare condition, of 
which a series of cases have been reported by McKernon. 7 

Treatment. —Most cases of acute tympanic disease are amenable in 
some degree both to general and to local treatment. We shall speak first, 
therefore, of such general measures as are of value in the management of 
any case of acute otitis media, and then of the local treatment appropriate 
to each of the two main varieties of the disease. 

General Treatment .—When the aural lesion occurs as a complication of 
some systemic disease (e.g., diphtheria, scarlatina, etc.), the general treat¬ 
ment must obviously include the treatment of that disease. When not 
secondary to an infectious disease, the general treatment resolves itself in¬ 
to an attempt to place the patient under the most favorable conditions for 
combating the local infection. In uncomplicated cases, this may be summed 
up practically in the following indications: (a) rest, (b) catharsis, (c) reg¬ 
ulation of the diet, and (d) hygienic arrangement of the sleeping room. 

ft est —By this is meant not merely absence from school or business, 
but absolute rest in bed. This favors recovery in two ways: (1) it secures 
freedom from the fatigues and excitements of the daily routine, which in 
the presence of an acute inflammatory lesion entail more than ordinary 
strain; and (2) it protects the patient from sudden changes in the peripheral 
body temperature. This is a matter of considerable importance in acute 
aural disease, where slight accessions of nasopharyngitis may cause rapid 
extension of the tympanic lesion. With children, it is particularly impor¬ 
tant and should be insisted upon. 

Catharsis .—In hospital practice, the routine treatment begins with the 
administration of some efficient laxative. Calomel in doses of gr. j to gr. 
iij according to the patient’s age, and followed in six hours by some drug 
acting more directly upon the intestines, gives the best results. This 
routine measure should be prescribed regardless of the presence or absence 
of constipation or digestive disorder. 


7 McKernon* Primary Jugular Bulb Thrombosis in Children as a Complication 
of Acute Purulent Otitis Media, N. Y. Med. Jour., July 1 and 8, 1905. 





172 ACUTE DISEASES OF MIDDLE EAR AND MASTOID 


Diet .—The digestive function is apt to be easily disturbed during the 
acute stage of any suppurative lesion. It is a common practice, therefore, 
to place a patient suffering with acute tympanic disease upon a strictly 
liquid diet. This, during the first twenty-four hours, is probably, in severe 
cases, a wise measure. As soon, however, as the patient begins to demand a 
more generous diet, it should be changed to a light diet of easily digested 
solid food, from which red meats should, at first, be excluded. Nothing 
is more senseless or irrational than to deplete the patient’s strength and 
powers of resistance by a prolonged starvation diet. 

Arrangement of the Room .—With most cases of acute tympanic disease 
there is a coexisting tubal catarrh with more or less pronounced naso¬ 
pharyngeal congestion. A room overheated tends rather to increase nasal 
congestion, and is as bad, if not worse, than one in which the temperature 
is too low. With the patient in bed, the room should be well ventilated, 
and the temperature in winter kept at about 60° to 65° F.,—the bed, of 
course, being so placed as to be protected from draughts. Unless these 
matters are arranged for by explicit directions, it will be no uncommon 
experience to find at one’s second visit all the windows closed and the 
temperature of the room at 75° or 80° F.,—a condition in itself capable of 
inducing pyrexia in one already ill. 

Non-operative Treatment of Acute Otitis Media .—By this is meant the 
management of a case of acute middle-ear inflammation without incision of 
the drum membrane. It is indicated in only a comparatively small per¬ 
centage of cases as they are first seen by the otologist. 

When inspection of the drum-head shows the lesion to be in the incip¬ 
ient stage, it may be advisable to try to abort the attack without incising 
the drum membrane. This is sometimes spoken of as the “abortive treat¬ 
ment.” It is admissible only in cases in which there are no evidences of 
pus accumulation or retention within the tympanum,— i.e., in which the 
drum membrane, though red, is not bulging. 

The abortive plan of treatment is as follows: The patient, whether 
child or adult, is at once ordered to bed. Calomel in dosage appropriate 
to the age is administered, and followed in six hours by some drug acting 
directly upon the bowels. This cleansing of the alimentary tract seems not 
only to prevent or relieve digestive disturbances, but also in some way to 
exert a favorable influence upon the tympanic lesion itself. 

To control pain while the abortive remedies are given time to act, 
the following prescription is of value, and in itself may influence the lesion 
favorably: 

B Codeinse, 

Extract, belladonna?, aa gr. j; 

Phenacetini, 

Salol, aa gr. xx. 

M.—Divid. in chart. No. viii. 

Sig.—One powder q. 4. h. 

During the first twenty-four hours the patient should be placed on a 
strictly liquid diet, which is then changed to a light diet of easily digestible 


TREATMENT OF ACUTE OTITIS MEDIA 


173 


food. Regular diet should be restored as soon as the lesion seems under 
control. It is certainly irrational to keep a patient suffering from acute 
middle-ear inflammation upon a continued starvation diet. 

Relief of Pain .—The meagreness of our resources for the relief of pain 
constitutes the weak point in this plan of treatment. Opium for the relief 
of the earache of acute otitis media is to be advised against for the reason 
that it would mask a very important guide as to the progress of the lesion. 
Locally our chief reliance is upon the application of dry heat, which, while 
it may not wholly annul a severe earache, often reduces very materially 
its intensity. While many appliances have been contrived for applying 
dry heat to the ear, none is more efficient than the ordinary hot-water 
bag. It should be only half filled with very hot water, wrapped with one 
or more layers of flannel, and the patient instructed to lie with the diseased 
ear in contact with it. With two bags in use, continuous application of 
heat is easily maintained. Poultices applied to the ear are said sometimes 
to affect the organ disastrously, and are never used in otological practice. 

When these measures seem at the end of twelve or twenty-four hours 
to have controlled the symptoms,— i.e., when the pain is relieved and 
inspection of the drum membrane reveals no evidences of pus accumula¬ 
tion within the tympanum,—the abortive plan of treatment should be 
continued. In cases responding favorably to this treatment, the pain 
usually subsides fairly promptly. The subjective noises, on the other 
hand, may be very persistent, and restoration of the drum membrane to 
its normal condition and appearance is often very gradual or slow. 

A possible disadvantage in this plan of treatment is illustrated in 
certain cases in which recovery, though ultimately complete, has been 
unduly delayed. There have been cases also in which, after a considerable 
period during which a favorable result seemed probable, incision of the 
drum membrane has finally become necessary on account of recurience or 
persistence of symptoms. 

When pain is not relieved within a reasonable period of time, or when 
the drum membrane, from having been simply injected, is seen to bulge 
into the canal from the pressure of pus or serum behind it, abortive meas¬ 
ures should be abandoned. 

That this plan of treatment is not more often put into practice by the otologist is 
due to two facts,—viz. (1) in most cases the patient does not come under his care and 
observation until after the lesion has passed the stage for which abortive measures are 
appropriate, and (2) the pain is often so great that the patient demands or requires 
immediate relief, and this is most promptly and safely secured by incision of the drum 

membrane. 

Surgical Treatment of Acute Catarrhal Otitis Media. W hen the lesion 
has advanced to the stage of pus formation and retention, it is clearly a 
surgical condition. The local treatment in such cases is logically based 
upon a recognition of two facts: (1) the necessity of providing free drain¬ 
age from the tympanum by means of an incision of the drum membrane, 
and (2) the necessity of keeping the external auditory canal as nearly as 


174 ACUTE DISEASES OF MIDDLE EAR AND MASTOID 


possible free of pus. We endeavor to carry out the second indication by 
(a) frequent irrigation of the meatus with sterile or antiseptic solutions, 
or (b) by capillary traction through gauze wicks or some form of sterile 
gauze dressing introduced into the meatus. 

Myringotomy. — When inspection of the ear shows the membrana 
tensa to be bulging (Fig. 102, p. 163), there should be no unnecessary 
delay in making a free incision through its posterior segment. This opera¬ 
tion, though occupying but a few moments, is exceedingly painful. It is 
much better, therefore, that the patient should be under the influence of a 
general anaesthetic. For this purpose nitrous oxide is the ideal drug, 
providing safe anaesthesia easily prolonged to the requirements of an 
operation on one or both ears, and usually leaving the patient absolutely 
without discomfort or untoward symptoms. The necessary steps in pre¬ 
paring the patient for operation are simple. Having been put to bed, 
where for the present he is to remain, the auditory canal is filled with 
peroxide of hydrogen. This is allowed to remain some three or four min¬ 
utes, the ear then being irrigated with a warm antiseptic solution,— e.g., 
bichloride of mercury 1 in 4000, or carbolic acid 1 in 200. A bit of sterile 
absorbent cotton or sterile gauze is introduced lightly into the outer 
extremity of the canal, and the patient is ready for the anaesthetic. 

Since our object is to evacuate pus presumably confined to the atrium, 
it is not either necessary or desirable that the incision should extend above 
the posterior fold so as to enter the vault. It is quite important, however, 
that the cut should be as extensive as possible within the limits of the 
membrana tensa. The posterior segment of the tense membrane is the 
broader, and is usually the part most markedly bulging in acute tympanic 
disease, and it is in the posterior segment that the incision is always made. 
A mere puncture of the drum membrane or a very short incision may bring 
temporary cessation of pain through relief of tension, but either closes 
prematurely or provides such inadequate drainage as not to insure the 

best results. Another unquestionable disadvantage 
of a mere puncture of the drum membrane is 
the fact that, even should it not close prematurely, 
it is much more apt to result in a permanent 
perforation than a more extensive incision. The 
incision should extend from the lower attachment 
of the posterior segment below to the middle of 
the posterior fold above (Fig. 109). 

Removal of Clot following Myringotomy .—Im¬ 
mediately following incision of the drum-head, 
there is always a free escape of blood into the mea¬ 
tus, and unless this receives attention, a clot may be 
left in the depths of the canal, partly or wholly defeating the purposes of 

the operation. I have known this to occur in cases left to the care 

of incompetent nurses. It is likely to occur, for example, if the first 

irrigation is delayed twenty minutes or more after the incision is 






TREATMENT OF ACUTE OTITIS MEDIA 


175 


made, and then the fountain bag instead of the hand syringe is used. 

I personally like to remain five or ten minutes after operating to see 
this post-operative clot, which is invariably present, dislodged. Once 
removed, it does not usually re-form. 

From this stage, the treatment is much the same as that described as 
the abortive method, plus measures for keeping the canal free of pus. 
The patient should be kept in bed, 8 placed upon liquid or very light diet, 
and the bowels freely moved. 

Irrigation .— During the first few days after myringotomy, the ear 
should be irrigated at rather frequent intervals with some antiseptic 
solution. Ordinarily, every three hours is often enough, but if the dis¬ 
charge becomes unusually profuse, syringing every two hours may give 
better results. Many bactericidal drugs have been advised by different 
authors, bichloride of mercury and boric acid being in most common use. 

Corrosive Sublimate in Aural Therapy .—Admitting that the use of this 
drug in solutions of proper strength is often followed by satisfactory results, 
there have in my experience been so many cases which seemed to be un¬ 
favorably influenced by it, that I am tempted to record my objections to 
its routine use. The unfavorable reactions as I have observed them may be 
mentioned in somewhat the following order: (1) In a certain small per¬ 
centage of cases corrosive sublimate even in weak solution has seemed to 
exert a distinctly destructive action upon the tissues, the incision in the 
drum membrane showing little tendency to heal, but rather to further 
enlargement by tissue disintegration. (2) There is a class of cases, par¬ 
ticularly numerous among children, in which a bichloride solution of 
any strength produces a dermatitis of the auditory canal and concha, 
resulting in an eczematous eruption which will persist so long as bichloride 
irrigations are continued. (3) Finally there have been cases in which the 
aural discharge has without other discoverable cause been unduly pro¬ 
longed, improvement following quickly upon a change of treatment. 

The use of this drug and the phenomena above described have seemed 
to me often to occupy a logical relation of cause and effect. Bichloride 
of mercury in 1 to 5000 solution, applied frequently to the hands, will 
produce a dermatitis. Taken into the stomach, it would not only prove 
toxic by absorption, but would quickly produce severe gastro-enteritis by 
its local action upon the mucosa. Entering the tympanum through the 
incision in the drum membrane, it is probable that the advantage derived 
from its bactericidal action is more than offset by its corrosive action upon 
the tympanic mucosa. Certainly many cases of acute otitis media- 
parti cularly in children—do better as soon as bichloride of mercury is 

discontinued. . . ,. . . 

Personally, the writer believes that in the cases m which routine irri¬ 
gation is successfully employed, its happy effects are due ui\ largely to 

8 While it is not always possible to insist upon confinement to bed in the case of a 
busy man or woman, there can be no doubt that it may play an important part in 
hastening recovery, and that its neglect is not without risks to the patient. 








176 ACUTE DISEASES OF MIDDLE EAR AND MASTOID 


its mechanical results in cleansing the meatus of pus, and only in minor 
degree to the germicidal action of the drug used in solution. He therefore 
prefers boric acid as less irritating than bichloride of mercury, and is 
inclined to believe that water absolutely sterilized by boiling might prove 
as effective as either. 

As soon as there is a noticeable diminution in the discharge, the fre¬ 
quency of the irrigations should be reduced, e.g., three times daily, twice 
daily, once daily, etc. 

Practical Suggestions .—I believe that every practical aurist will agree 
with me that the value of routine irrigation in acute middle-ear disease 
depends much less upon the frequency than upon the thoroughness of the 
irrigation. The object in view is simply the complete removal of pus from 
the meatus. If this can be accomplished by a single forcible compression 
of a small rubber syringe, we gain nothing by repetition of this procedure. 
If the contents of a vessel containing two quarts— e.g., the rubber bag of 
the ordinary fountain syringe—have been allowed to flow in and out of 
the ear, leaving a residue of thickened pus at the fundus of the canal, 
nothing of value to the patient has been accomplished. With an adult, 
some form of hand syringe by which current force can be controlled gives 
satisfactory results. The auricle should be drawn somewhat upward and 
backward, and a stream of some force directed along the posterosuperior 
canal wall toward the drum membrane. Properly used, the contents of 
an ordinary coffee-cup usually suffice thoroughly to cleanse the canal of 
pus. After the irrigation, a ball of sterile absorbent cotton should be placed 
in the concha (not introduced into the meatus), and the head turned side¬ 
ways so that the irrigated ear is directed downward. The cotton is removed 
as soon as the surplus moisture from the irrigation has been absorbed. 

With nervous or very young children, the hand syringe is often diffi¬ 
cult for the nurse to manage effectively, and then the fountain syringe 
may be used instead. When the fountain syringe is employed, it is better 
to use a larger quantity of water,— i.e., one or two quarts,—and the bag 
should be held or secured on an elevation at least three feet above the 
patient’s head. 

I have known a vigorous infant to resist even the fountain syringe so 
effectively as to make irrigation very difficult even by this method. In 
such a case the child should be tightly wrapped in a sheet, the hands and 
arms being pinioned to the side of the body, and the sheet held by safety- 
pins. By this procedure resistance is rendered impossible, and it is sur¬ 
prising how soon the most unmanageable child realizes the painlessness of 
the measure and ceases to object to it. 

No matter how carefully the nurse may perform her duties, it will be 
found that the fountain syringe will in certain cases leave a residue of 
thickened pus at the bottom of the canal. This is a common cause of 
failure in children. It is due often to the thick, adhesive character of the 
pus rather than to a faulty method of syringing the ear. This difficulty 
may be eliminated by preliminary use of a few drops of hydrogen peroxide 


TREATMENT: CAUSES OF FAILURE 


177 


poured into the meatus and allowed to remain four or five minutes pre¬ 
vious to the irrigation. The value of the peroxide is not so much from its 
bactericidal action as from its power of dissolving thickened secretions at 
the fundus of the canal, thus facilitating their expulsion. The theory that 
this use of peroxide of hydrogen may cause a spread of the infection by the 
evolution of gas within the tympanum is not supported by any observed 
facts in actual practice. 

When satisfactory results do not follow the irrigation method of cleans¬ 
ing a discharging ear in acute tympanic disease, we should look for a pos¬ 
sible cause of failure in one or other of the following conditions, viz.: 

1. Faulty Technic. — Direct the nurse to irrigate the ears as usual, 
and immediately thereafter examine the ears by speculum and reflected 
light. If a residue of pus remains in the depths of the canal, the procedure 
is worse than useless. This is undoubtedly a common cause of failure. 

2. The discharge may be so profuse as to require more frequent irri¬ 
gations than are being employed. In this case, increasing their frequency 
to the point necessary to keep the meatus free of pus may give better 
results. 

3. The incision in the drum membrane may have prematurely closed 
to a point no longer adequately draining the tympanum. While gradual 
closure of the perforation belongs to the normal process of repair, yet, if it 
occurs without proportionate diminution in the amount of pus secreted, a 
second incision of the drum membrane may be necessary. 

4. Finally, there are certain cases in which one is forced to conclude 
that frequent irrigations tend to retard tympanic resolution. Such a 
conclusion being reached, the irrigations should be discontinued or modi¬ 
fied by combination with other measures. 

Wick Treatment in Acute Otitis Media. — Personally I believe that 
there sre few cases of acute middle-ear inflammation which do not sooner 
or later reach a stage in which the wick treatment may with advantage be 
substituted for irrigation, or combined with it. By this method we depend 
partially upon capillary traction by means of sterile gauze to take up the 
pus draining into the meatus. 

Teclmic. — Free drainage from the tympanum being assured, the 
meatus is cleansed by means of pledgets of sterile absorbent cotton wound 
about applicators,—first dry and then dipped in alcohol. A prepared 
wick or strip of absolutely sterile gauze is then carefully introduced into 
the meatus so that its end is in contact with the perforation in the drum¬ 
head. The whole canal is thus filled with gauze, lightly packed. The 
outer end of the wick or gauze strip should not protrude from the meatus. 
The concha should now be filled with a small pad of sterile absorbent 
cotton. In the case of a restless child or nervous adult, who would be 
likely to disturb this dressing, the wick may be allowed to protrude from 
the meatus, and this and the whole ear may be covered with handkerchiefs 
of sterile gauze such as are used in covering a mastoid wound, the whole 
being held in place by a narrow gauze bandage. With the average intel- 

12 


178 ACUTE DISEASES OF MIDDLE EAR AND MASTOID 


ligent adult, however, the simpler dressing answers every purpose and 
possesses some advantages. Within twelve to twenty-four hours, this 
dressing should be removed and the wick carefully examined for the amount 
of pus that has come away with it. Frequently the wick and cotton in the 
concha are found completely saturated with pus at the first change of 
dressings. This, of course, is what one would expect.. The meatus is now 
cleansed as before with alcohol and sterile absorbent cotton, and the drum 
membrane inspected to make sure that the incision is not prematurely 
closing. Drainage being adequate and the patient’s general condition 
being satisfactory, a sterile wick exactly similar to the first should be 
applied. These dressings should be changed at regular intervals of twelve 
to twenty-four hours, according to the copiousness of the discharge. Each 
dressing removed should be carefully scrutinized for changes in the amount 
of pus. In a favorable case, a distinct diminution will soon be noticeable. 
The use of wicks may be combined with irrigation by syringing the ear at 
each change of dressing, a plan which often gives exceedingly satisfactory 
results. In some cases it will be found necessary to abandon the use of 
wicks altogether. In the writer’s hands, however, it has been of undoubted 
value in shortening many attacks, and he is convinced that it has turned 
the scale in some cases which were not progressing favorably. 

The chief disadvantages in the wick treatment are the difficulties in 
correctly carrying out its provisions. It can be employed safely only in 
such cases as can be kept under the physician’s close personal care and 
supervision. The writer regards it as contra-indicated in (a) acute infec¬ 
tious diseases complicated by acute middle-ear inflammation, and (b) in 
cases of acute tympanic disease accompanied by high fever or other signs 
of septic absorption. 

Catheter Inflation in Acute Tympanic Disease .—The Eustachian cathe¬ 
ter has a distinct field of usefulness in the treatment of acute middle-ear 
inflammation. That it is so seldom used is due probably to the fear that 
the current of air may carry pus from the tympanum into the mastoid 
cells. This, in the writer’s opinion, is a remote possibility. In the normal 
ear the atrium is more or less separated from the vault by the structures 
massed at the boundary line between the two (see Fig. 27). During an 
acute middle-ear inflammation the swelling of the tympanic mucosa must 
tend to render this separation more complete. If inflation were performed 
in a case in which no adequate opening in the drum membrane had been 
provided, it is possible that harm might result from the displacement of 
pus. After free incision of the drum-head, however, it seems clear that air 
entering the tympanum from the Eustachian catheter must find its path 
of least resistance through the incision in the drum-head, carrying with it 
some of the pus or fluid in the tympanum. Upon physical grounds, there¬ 
fore, it would seem that catheter inflation may be used to advantage in 
certain stages of acute tympanic inflammation. For example, when 
diminution in the amount of discharge has warranted us in reducing the 
number of irrigations to twice or three times daily, we have reached a 


TREATMENT OF ACUTE PURULENT OTITIS MEDIA 179 


point from which further progress is in some cases rather slow. Suppose, 
in such a case, that after irrigation we inspect the drum membrane and, by 
wiping out residual moisture, satisfy ourselves that the canal is free of 
pus. We may now cleanse the nose and nasopharynx by alkaline sprays 
and carefully inflate the ear by catheter, using not 
too much force. If subsequent inspection shows a 
residue of pus thrown out into the meatus, we may 
easily wipe this out with sterilized cotton. If now 
we introduce a sterile gauze wick into the canal and 
leave this in contact with the drum-head to take up 
pus as it escapes through the perforation, it is clear 
that we have left both canal and tympanum in a con¬ 
dition more favorable for prompt resolution than 
if irrigation alone were depended upon. I am con¬ 
vinced that the course of the disease may in many 
cases be materially shortened by these measures. 

Treatment of Acute Purulent Otitis Media .—The treatment of acute 
suppurative otitis media may be dealt with briefly, since it is necessary 
only to point out wherein it differs from that of the milder form. In the 

first place, there is no stage of 



Fig. 110. — Incision indi¬ 
cated in acute purulent otitia 
media. 


the disease for which palliative, 
or abortive, measures are either 
adequate or safe. Infection of 
the vault is in itself an indication 
for incising the drum membrane. 
In practically all cases, therefore, 
the treatment begins with a myrin¬ 
gotomy. The incision should begin 
near the lower marginal attach¬ 
ment of the posterior segment 
below, and extend upward to and 
through the posterior fold so 
that the knife may enter and 
provide drainage from the vault 
(Fig. 110). When, in addition 
to the inflammatory changes in 
the drum membrane, the postero- 
superior canal wall is noticeably 
inflamed or swollen, this also 
should be incised. This is accom¬ 
plished by rotating the knife 
so that its cutting edge is directed 
backward, and dividing the adjacent inflamed portion of the canal 
wall as the blade is withdrawn (Fig. 111). This inflammatory condition 
of the meatus resulting from acute suppurative otitis media is prac¬ 
tically always confined to the soft parts covering the posterosuperior 



Fig. 111.—Incision through drum-head and 
posterosuperior canal wall. 













180 ACUTE DISEASES OF MIDDLE EAR AND MASTOID 


wall of the bony meatus. The incision, to give maximum relief, should 
divide all tissue down to the bone. 

Following myringotomy, the measures advocated for the milder form 
of the disease are of equal or even greater importance here. Absolute rest 
in bed, catharsis, and careful regulation of the diet may exert a decided 
influence upon the course of the disease, or at least upon the duration 
of the attack. The ear should be irrigated every three hours with a 
sterile or antiseptic solution,—a boric acid solution (dr. ss ad oz. viij) being 
the writer’s preference. Later, when the amount of the discharge has 
become noticeably diminished, the frequency of the irrigation should be 
reduced,— e.g., to one, two, or three times a day. I believe that the ear 
should not be syringed oftener than is necessary to keep the canal fairly 
free of fluid pus. With diminution in the amount of the discharge, the use 
of gauze wicks may be combined with periodic irrigation. By this plan 
the ear is irrigated once or twice daily,—once being usually sufficient,— 
the canal in the interim being filled with a strip of sterile gauze. In addition 
to the above measures, occasional catheter inflation to clear the atrium 
and hypotympanic space will influence some cases favorably. It must be 
employed with care,— i.e., with only moderate force,—and only after the 
acute stage is well passed, the physician having assured himself that an 
adequate opening in the drum membrane remains. The objection that 
inflation, even though practised with gentleness, may in these cases carry 
pus from the antrum to the mastoid cells is, I believe, founded on theory 
rather than fact. 

Antrum Tenderness. —At the height of an acute suppurative otitis 
media of average severity, some degree of tenderness over the antrum is 
usually present. This physical sign undoubtedly denotes an extension of 
the inflammatory process from the tympanic vault backward to the ant¬ 
rum, but does not necessarily mean suppurative involvement of the mastoid 
cells proper. I believe that this condition— i.e., tenderness localized over 
the antrum arid occurring early in a suppurative middle-ear lesion—is 
one for which the application to the mastoid of the ice-bag or Leiter’s coil 
may be of positive value in limiting the process and preventing spread 
of infection throughout the mastoid cells. All, however, that can be 
accomplished by its use is obtained by twenty-four hours of continuous 
application, after which it may be distinctly harmful in lowering the 
vitality of the part. 

Occasional Necessity for Re-incising the Drum Membrane. —The normal 
drum membrane exhibits a remarkable tendency to rapid healing after 
puncture or incision, provided infection has not occurred. I have seen a 
drum membrane, after free incision for the relief of severe earache in the 
initial stage of acute catarrhal otitis media, practically healed at the end 
of forty-eight hours. This tendency to quick healing occasionally works 
to our disadvantage in the treatment of acute purulent otitis media, in 
which closure of the incision advances more rapidly than repair of the sup¬ 
purative process within the tympanum. I wish to emphasize the fact that 


ACUTE MASTOIDITIS 


181 


in cases of retarded resolution following myringotomy, if inspection shows 
that the opening in the drum-head is no longer affording adequate drain¬ 
age, there should be neither hesitation nor delay in re-incising the mem¬ 
brane. Nor can we formulate any rule as to the number of times it may be 
necessary or wise to repeat this operation. Even in cases in which my¬ 
ringotomy has been repeated one or more times, should evidences of pus 
retention within the tympanum recur, reopening of the drum membrane 
will often lead to recovery. There can be no doubt that delayed resolution 
is due in a certain proportion of cases to the fact that the individual’s 
vitality or power of resistance is below par, and it is a reasonable hypoth¬ 
esis that the same causes might unfavorably influence the process of repair 
following operation upon the mastoid. 

The measures outlined above, if thoroughly and conscientiously carried 
out, will bring about recovery in all cases of acute middle-ear inflammation 
except in those in which the process of repair is interrupted by one or 
other of the following conditions: 

(a) Acute suppurative mastoiditis. 

(b) Caries of tympanic structures leading to the condition known as 
chronic suppurative otitis media. 

(c) Spread of the infection to the labyrinth or to one or other of the 
intracranial structures. The syniptoms by which such extension of the 
disease is announced will be discussed in connection with the lesions 
mentioned. 

After Treatment .—After the discharge has ceased and the drum mem¬ 
brane is completely healed, the after treatment, if any be required, is the 
same whether the lesion has been of the catarrhal or purulent type. If 
the hearing is perfect and no subjective symptoms persist, no treatment is 
called for. On the other hand, if tinnitus or other subjective symptoms 
persist, or if the hearing remains below par, it may be necessary to practise 
occasional inflation by catheter to break up newly formed adhesions and 
correct any remaining congestion within the tympanum and Eustachian 
tubes. Quite often, however, these conditions correct themselves without 
treatment. 

ACUTE MASTOIDITIS. 

Etiology. —Acute suppurative mastoiditis is practically always sec¬ 
ondary to a suppurative lesion of the middle ear. W hile cases have been 
reported in which the drum membrane has presented no signs of inflam¬ 
mation, past or present, there is no evidence in such cases that a tympanic 
lesion has not preceded, and given rise to, the mastoid disease. Primary 
mastoiditis due to syphilitic or tubercular infection, while theoretically 
conceivable, is so rare as to be practically negligible. It is not seen in 
actual practice. Traumatic mastoiditis is among the rarest lesions. In 
short, the mastoid process seems to enjoy immunity from acute disease 
except as a result of infection from a diseased tympanum. 

Pathology. —We shall obtain a much clearer conception of the pa- 


182 ACUTE DISEASES OF MIDDLE EAR AND MASTOID 


thology of this rather grave lesion if we bear in mind two facts, namely: 
(1) The so-called mastoid antrum should not be regarded as one of the 
mastoid cells, but simply as the posterior end of the tympanic vault. In 
the foetus at term, the mastoid process as such does not exist, yet the 
antrum is already a large and easily demonstrable cavity. (2) In acute 
purulent otitis media, the inflammatory process and the flow of pus must 
quickly invade the antrum. This, however, does not of itself constitute a 
true suppurative mastoiditis. Acute mastoiditis may be defined as an 
acute inflammatory process originating in the antrotympanic cavity and 
spreading thence to the mastoid cells proper. It is probable that the in¬ 
flammatory process passes in most cases through certain fairly well defined 
stages,—viz. (1) stage of vascular engorgement and cell infiltration; (2) 
suppurative stage, characterized by the presence of fluid pus; and (3) the 
stage of osseous necrosis or softening. These three stages are clearly and 
easily recognized macroscopically during operations upon patients in dif¬ 
ferent stages of the disease. 

Probably there is no well recognized lesion which presents such wide 
variations in the rapidity or slowness with which the disease advances. 
Thus, in one case weeks may elapse without the development of symptoms 
justifying a decision to operate, while in another case, operated upon but 
a few days after the onset of the tympanic disease, the cells throughout the 
mastoid may be bathed in pus. If one will refer to Plate III, page 33, 
showing recognized structural variations, or types, of the normal mastoid,— 
or, better still, if one will examine any fairly large series of bone sections,— 
these variations in the pathology of the disease will be more easily under¬ 
stood. Thus, it is clear that in a temporal bone characterized by a large 
antrum in close relation to large pneumatic spaces separated only by thin 
lamellae of bone, a suppurative process would logically advance with far 
greater rapidity than in a bone presenting a very small antrum and a 
sclerotic mastoid. 

On exposing the mastoid cortex, we find in a majority of cases no 
changes indicative of the pathologic changes within the bone. In adults, 
only if the lesion is of comparatively long duration, are cortical per¬ 
forations likely to be present. The most common site of such cortical 
defects is the space slightly above and behind the spine of Henle; but 
they may occur at any point upon the outer cortex from the temporal 
ridge above to the tip below. Perforation may also occur through the 
thin bony plate forming the inner covering of the mastoid tip (Bezold’s 
perforation or abscess). 

In young children, owing to the comparative thinness and softness of 
the outer covering, cortical perforations are by no means uncommon. 

On removing the cortex, we may find any of the following conditions, 
which, in the order named, represent roughly the successive stages of 
the lesion: (a) Antrum more or less filled with fluid pus draining back¬ 
ward from the tympanic vault. The mastoid cells contain no pus, 
but their mucous lining is red, swollen, and bleeds easily and pro- 


ACUTE MASTOIDITIS: SYMPTOMS 


183 


fusely, showing great vascular engorgement. (b) Cells adjacent to the 
antrum, and also the large cell at the tip, contain a variable amount 
of fluid pus. (c) Mastoid cells throughout contain pus and exuberant 
granulations, (d) Intercellular bone substance is softened or completely 
disintegrated, (e) In the later stages necrosis of the intercellular bone 
substance may co-exist with intact inner plates, or the latter may exhibit 
areas of necrosis. 

Pus, being present within the mastoid, may be removed wholly or in 
part by absorption through the lymphatics, or may find a pathway of 
escape through perforation of the bone brought about through osseous 
necrosis. The various pathways of escape, and the lesions to which they 
give rise, will be spoken of in a later chapter. 

Symptoms. —The symptoms of acute mastoiditis are usually engrafted 
upon those characteristic of acute purulent otitis media. W e have, there¬ 
fore, to ask ourselves what symptoms, or modifications of symptoms, 
occurring during an attack of acute middle-ear suppuration, or duiing 
convalescence therefrom, should lead us to suspect suppurative involve¬ 
ment of the mastoid cells. 

Pain and Insomnia .—The patient, who has been comparatively com¬ 
fortable, may suddenly experience deep-seated pain in the region of the 
mastoid process. Or, in the absence of actual pain, there may be a dis¬ 
tressing sense of fulness, soreness, or discomfort referred to the mastoid. 
On the other hand, there are many cases in which the patient complains 

little either of mastoid pain or discomfort. 

In the presence of mastoid pain or discomfort, and in proportion to its 
severity, insomnia is usually present, and sudden inability to sleep at 
night is in some cases a useful guide to arrested resolution. 

Fever .—Elevation of temperature, usually of moderate degree, may 
be more or less continuously present during suppurative disease of 
the mastoid. When present it is a most important symptom, and 
one which, unless yielding fairly rapidly to rational non-operative 
measures, calls more or less imperatively for surgical intervention. 
Fever, however, is in one sense a most unreliable symptom, in that 
many cases of severe mastoiditis exhibit throughout no noticeable 
elevation of temperature. That extensive necrosis of the mastoid cells 
may coexist with a practically normal temperature cur\ e is a fac t 
now fortunately recognized. In the author’s experience fever is absent, 
or so slight as to be of no special diagnostic value, in a majority of 
cases. Absence of fever is, therefore, no evidence that the mastoid 
cells are not extensively diseased. 

Aural Discharge— The aural discharge may undergo certain quantita¬ 
tive changes which would lead an experienced aurist to suspect mastoid 
involvement. For example, a rather copious discharge may suddenly 
cease, this abrupt cessation being accompanied by no amelioration of the 
patient’s condition and being followed within a few days or hours by a 
renewed flow of pus. Or, again, a moderate discharge may suddenly or 


184 ACUTE DISEASES OF MIDDLE EAR AND MASTOID 


gradually increase in volume until it becomes necessary upon purely 
physical grounds to assume involvement of the mastoid cells in order to 
explain the amount excreted in the twenty-four hours. In still another 
group of cases, the long persistence of the discharge may of itself force the 
inference of a focus of disease beyond the limits of the small tympanic 
cavity. 

Changes in the Drum Membrane and Sagging of the Posterosuperior 
Canal Wall. —While cases have been observed in which the tympanic 
condition has improved simultaneously with the advance of a suppura¬ 
tive process within the mastoid, such cases are exceedingly rare. As a 
rule, the drum membrane presents the picture of severe suppurative 
otitis media. It is usually perforated, red, and markedly bulging 
in the upper posterior quadrant. That these tympanic changes are 
often a result of the disease within the mastoid is frequently demon¬ 
strated by the rapidity with which the diseased drum membrane 
regains its normal condition and appearance after operation upon the 
mastoid. A very common feature of these cases is a noticeable inflam¬ 
matory thickening of that portion of the posterosuperior canal wall 
which immediately adjoins the drum membrane, so that the one 
gradually merges into the other, there being no distinguishable line of 
demarcation between the two. This is undoubtedly due to a periostitis 
in this situation, and is so frequently seen in cases of acute purulent 
otitis media complicated by mastoid suppuration that it is by some 
authors regarded as pathognomonic of the latter condition. Taken in 
connection with other symptoms, it is of considerable diagnostic value; 
alone, it is not a reliable sign of mastoid disease. 

Mastoid Tenderness. —Undoubtedly the most reliable sign of acute 
mastoid disease is sensitiveness to pressure over the mastoid cortex. This 
varies in different cases from moderate tenderness elicited only by firm 
pressure to extreme sensitiveness even to very light pressure. In some 
degree it is usually present in every case of suppurative mastoiditis. In 
many cases it seems to reach its height during the early (vascular) stage, 
becoming less marked as these initial inflammatory changes are past. 
Most aural surgeons have been occasionally surprised in operating upon 
cases in which intense mastoid tenderness has been present to find an 
absence of pus, the most conspicuous macroscopic change being extreme 
vascular engorgement. During the later progress of the lesion, exacer¬ 
bations of mastoid tenderness may occur, being due probably to an 
occasional extension of the inflammatory process to cells not hitherto 
involved, or to the influence of pus temporarily retained under pres¬ 
sure in certain cells. 

Undoubtedly, the degree of mastoid tenderness is in some degree 
related to the type of bone involved. For example, it seems a logical 
deduction that a suppurative inflammation involving a mastoid process 
of thin cortex and pneumatic structure (see Plate III, page 33) would 
give rise to greater sensitiveness to pressure than would a similar process 


ACUTE MASTOIDITIS: SYMPTOMS 


185 


within a sclerotic mastoid, or one having a very thick cortex. From this 
relation, one may in some cases reach a practical inference from one’s 
clinical data as to the type of the diseased mastoid, and therefore as to 
the character of the lesion. Thus, in a case in which symptoms of mastoi¬ 
ditis with very marked mastoid tenderness follow rapidly upon the onset 
of the tympanic lesion, one may infer with considerable confidence that 
one has to deal with a pneumatic mastoid having a comparatively thin 
cortex. On the other hand, with symptoms of more gradual development 
and with well-marked mastoid pain or discomfort coexisting with very 
slight sensitiveness to pressure, one would expect to find a mastoid of 
sclerotic type, or one having a thick cortex. Clearly the latter may be the 
more serious condition. 

It will be seen from what has been written that the clinical picture 
includes only a limited number of symptoms which can be said strictly to 
characterize the disease. 

To epitomize: The symptoms to be looked for are mastoid pain, with 
consequent insomnia; elevation of temperature; certain quantitative changes 
in the character of the discharge; mastoid tenderness, and bulging of the pos- 
terosuperior canal wall. The above rather meagre clinical picture may be 
said to comprise practically all the symptoms which are characteristic of 
an uncomplicated case of acute mastoiditis. 

Unfortunately, many cases of acute mastoiditis run their course with 
complete absence of one or more of the above symptoms. For example, 
neither elevation of temperature nor mastoid pain may be present. When 
fever is absent and pain inconsiderable, the subjective and constitutional 
phenomena are naturally not very characteristic. Even in such cases, 
however, there is usually some feature in the clinical picture which will 
cause the experienced observer to suspect that recovery is being inter¬ 
rupted by the advance of a suppurative process within the mastoid. For¬ 
tunately, there is one physical sign which is seldom or never wholly absent. 
Some difference in the sensitiveness of the two mastoids to pressure can 

usually be demonstrated by careful palpation. 

There remain to be described certain changes in the position of the 
auricle and in the contour of the soft parts about the ear, w hich are among 
the more unusual accompaniments of mastoid inflammation. Auricular 
displacement is a comparatively rare result of mastoid inflammation in 
adults. When present it constitutes a very characteristic deformity. It 

may be produced in one of two ways, viz.: 

(1) Subperiosteal Abscess .—'The suppurative process within the mas¬ 
toid gives rise to a perforation in the mastoid cortex. Pus escaping through 
this perforation elevates the periosteum from the surrounding bone, and, 
being confined beneath the periosteum, constitutes what is known as a 
subperiosteal abscess. As this abscess is usually in close proximity to the 
posterior attachment of the pinna, the postauricular sulcus is often 
obliterated and the auricle markedly displaced. If the perforation is 
behind the centre of the postauricular attachment, the auricle is pushed 


186 ACUTE DISEASES OF MIDDLE EAR AND MASTOID 


directly forward, standing prominently outward from the side of the 
head. When the perforation is at a higher level, the auricle is displaced 
both forward and downward (Fig. 112). 

(2) Postauricular (Edema .—In another class of cases the acute inflam¬ 
matory process extends through the mastoid cortex without causing a 
perforation. This extension of inflammation involves the periosteum and 
overlying soft tissues, which become markedly swollen or oedematous. 
This condition gives rise to a deformity similar to that above described, 
though usually less pronounced. 

While auricular displacement is in adults comparatively rare as a result 
of mastoiditis, it occurs very frequently in the mastoiditis of infants and 
young children. It will also be recalled that a similar deformity is a very 
common feature of furunculosis of the meatus in adults. The two lesions 
are very different, however, in their surgical significance, for whereas the 
postauricular oedema and consequent displacement resulting from furun¬ 
culosis of the canal are usually relieved by incision of the focus or foci 
of infection within the meatus, the subperiosteal abscess or oedema result¬ 
ing from mastoid suppuration is a positive indication for opening the mas¬ 
toid. Hence the importance of being able to make a correct diagnosis. 
It may be well therefore to repeat briefly the chief differential points be¬ 
tween the two conditions. 

Auricular Displacement 
in Furunculosis. 

1. Common in adults; rare in children. 

2. Pain always severe; increased by 
movements of the jaw. 

3. Any manipulation of the auricle 
causes excruciating pain. 

4. Speculum examination shows fu¬ 
runcular swelling situated always in fibro¬ 
cartilaginous portion of canal. 

5. Drum membrane may be, and usu¬ 
ally is, intact. 

6. Discharge, if present, comes from 
furuncular perforation in membrano-car- 
tilaginous canal. 

7. Pressure upon the mastoid, so di¬ 
rected as not to move or disturb the auri¬ 
cle, causes no pain. Pressure at same 
point, but directed slightly forward so as 
to disturb the auricle, causes great pain. 

Bezold's Abscess .—A more unusual complication of suppurative 
mastoiditis was first described by the late Professor Bezold, and is known 
as a Bezold abscess. This condition is caused by a perforation in the bony 
plate forming the inner surface of the tip of the mastoid. It occurs pre¬ 
sumably in cases in which the tip cells are especially large and in which 


Auricular Displacement 
in Suppurative Mastoiditis. 

1. ^ ery common in children; com¬ 
paratively rare in adults. 

2. Pain not usually severe, and may 
be absent; not influenced by movements 
of the jaw. 

3. Manipulation of the auricle causes 
absolutely no pain. 

4. Inspection of meatus shows absence 
of inflammation in fibrocartilaginous part 
of canal. Inflammation, if present, con¬ 
fined to lining membrane of posterosupe- 
rior wall of bony canal. 

5. Drum membrane almost invariably 
perforated. 

6. Discharge from the tympanum 
through perforation in drum membrane. 

7. Pressure upon the mastoid elicits 
deep bone tenderness. 


Fig 112—Auricular displacement resulting from postauricular subperiosteal absces 

























MASTOIDITIS IN INFANTS AND YOUNG CHILDREN 187 


the bony plate forming the inner or medial wall of the tip is very thin, 
and the outer cortex thick. Pus escaping through such a perforation 
burrows downward in the neck beneath the sternomastoid, or may be con¬ 
fined between layers of the deep cervical fascia. It presents a prom¬ 
inent, elongated swelling below the mastoid in the neck, which, if other 
symptoms of mastoid disease were not clear, might present difficulties of 
diagnosis. It renders the surgical treatment of the disease rather more 
troublesome by the occasional necessity of extensive incisions in order to 
provide adequate drainage from the cervical spaces involved. 

Paralysis of the Abducens (6th) Nerve .—A somewhat puzzling compli¬ 
cation, which the aurist has sometimes to deal with, is the development dur¬ 
ing the course of a suppurative mastoiditis of paralysis of the 6th cranial 
nerve. It will be recalled that this is purely a motor nerve and that it 
supplies only one muscle, the external rectus muscle (occuli). 

Origin and Position .—According to Gray, the deep origin of the 6th 
nerve is from the gray substance of the fasciculus teres by a nucleus com¬ 
mon to it and to a part of the 7th (facial) nerve. It is said also to be con¬ 
nected with the nuclei of the 3rd and 4th nerves. Its superficial, or appar¬ 
ent, origin is from the upper constricted portion of the medulla just behind 
the pons. The trunk, as it passes forward along the inner wall of the cav¬ 
ernous sinus to enter the orbit through the foramen lacerum anterius is in 
more or less close relation with the molar occuli (3rd), the pathetic (4th) and 
the ophthalmic branch of the trifacial (5th). It is also in relation with the 
cavernous portion of the internal carotid artery. Within the orbit it is 
distributed solely to the inner surface of the external rectus muscle, con¬ 
traction of which rotates the eye outward. 

Pressure by tumors, the exudates of a basilar meningitis or of cerebro¬ 
spinal syphilis may disturb its function. 

The diagnosis of 6th paralysis is simple. The patient usually com¬ 
plains of the discomforts incident to double vision. When any small object, 
e.g., a pencil, is held directly in front of him,— i.e., in the median plane of 
vision,—it is seen as a single object. So also when it is moved laterally 
in the direction corresponding to the sound nerve. When, however, it is 
moved in the opposite direction, diplopia is complained of as soon as the 
median plane of vision is passed, when it will be seen that the eye corre¬ 
sponding to the paralyzed nerve remains stationary in the median position, 
while the sound eye follows the moving pencil as normally. 

The path of infection from mastoid to 6th nerve is usually obscure. 
Theoretically, one may say (1) that the nerve may be compressed 
by disease (thrombosis) of the cavernous sinus; (2) that it may be subjected 
to pressure by a thrombus in the anterior end of the inferior petrosal sinus 
(Page’s case 9 ); (3) that the nerve sheath maybe involved in a meningitis 
spreading inward from a necrotic tagmen antri; (4) that a suppurative 
labyrinthitis may give rise to a subtentorial leptomeningitis which, extend¬ 
ing forward, may involve the nerve sheath; (5) that the nerve lesion may be 

9 Page: Thrombosis of Jugular Bulb; Paralysis of External Rectus Occuli; Annals 
of Otol. Rhinol. and Laryng., June, 1910. 




188 ACUTE DISEASES OF MIDDLE EAR AND MASTOID 


an extention by continuity from disease involving the apex of the petrous 
bone (Gradenigo). While some of these roadways of infection seem to have 
been definitely established in recorded cases, they are usually in actual 
practice merely hypotheses, which do not throw much light upon the path¬ 
ologic aspect of the case in hand. In 1918 the author 10 published the history 
of a case in which a paralysis of the 6th nerve which had existed at least 
two weeks, disappeared completely on the third day after a mastoid oper¬ 
ation; but the pathway of infection could not be determined. The number 
of such cases which have been recorded is quite large. 

In 1910 Dr. C. E. Perkins 11 of New York published a very interesting 
review of the literature of this subject up to that time. His report embraced 
sixty cases, in twenty-nine of which, the mastoid was operated upon, no 
operation having been performed in the remaining thirty-one cases. Of the 
cases operated upon, there were one death, one failure (■ i.e ., of restoration of 
nerve function) and twenty-seven complete recoveries. Of the thirty-one 
cases treated non-surgically there were four deaths, three failures and 
twenty-five (sic) recoveries. So far as any deductions are permissible from 
these figures, they would seem to be; that in suppurative mastoiditis 
associated with 6th nerve paralysis, the mortality is far greater and the 
percentage of 6th nerve recoveries far less in cases not operated upon than 
in those in which a mastoid operation has been performed. The author 
believes, therefore, that even in cases in which the symptoms referable to 
the mastoid are not very marked, the association of a homolateral para¬ 
lysis of the external rectus muscle should be regarded as a positive indica¬ 
tion for the mastoid operation. 

Gradenigo’s Symptom-Complex. —Before leaving the subject of abducens 
paralysis a word should be said as to the surgical import of what is known as 
Gradenigo’s symptom complex. Gradenigo attributed to it a surgical 
significance only in the presence of a suppurative lesion of the mastoid. 

This complex is present when with evidences of middle ear or mastoid 
infection, there is associated a homolateral paralysis of the 6th nerve,, eye 
pain or facial neuralgia and also severe frontal headache. This is thought 
to point strongly to necrosis or at least to a suppurative lesion of the apex 
of the petrous bone. 

It is clear that such a diagnosis would place upon the surgeon a very 
grave responsibility. It is important to bear in mind, therefore, that this 
syndrome might easily represent the combined results, or symptoms, of 
separate and distinct lesions. For example, should mastoiditis co-exist, as 
is not very uncommon, with suppurative disease of the ethmoid cells or 
sphenoid sinus, it is quite conceivable that the abducens paralysis might 
be a product of the mastoid lesion, while the sensory components (eye pain, 
facial neuralgia, frontal headache) might have their origin solely in the 
diseased ethmoid or sphenoid. 

Mastoiditis in Infants and Young Children . —Before leaving the sub- 

10 Kerrison: A case of abducens paralysis complicating mastoiditis: brief discussion 
of this complication as a surgical indication; Medical Record, November 30, 1918 

11 Perkins: Abducens Paralysis and Otitis Media Purulenta; Annals of Otology, 
September 1910 





MASTOIDITIS IN INFANTS AND YOUNG CHILDREN 189 

ject a word should be said as to the symptoms as observed in young children. 

Since the mastoid process as such does not exist during the first months 
of infantile life, it seems paradoxical to speak of mastoidectomy as occa¬ 
sionally called for at this period of development. It is an established 
clinical fact, however, that even in the first months of life, acute middle- 
ear inflammation may give rise to necrosis of the outer wall of the antrum 
and consequent subperiosteal abscess, and this condition for convenience 
of description is spoken of as mastoiditis. Antritis would be a scientifically 
more correct term. 

The symptoms of mastoiditis in infancy and early childhood resemble 
those of adult life, with the following differences: 1. The child suffering 
from acute aural disease is usually unable to differentiate between pain 
referred to the antrum and pain localized in the tympanum. Antrum pain 
is therefore of little diagnostic value in determining mastoid inflammation. 

2. Fever is usually present rather persistently duiing the acute stage 
of an acute purulent otitis media. After its recession a subsequent rise 
of temperature may easily be due to a slight exacerbation of the tympanic 
lesion. Fever, therefore, is hardly a reliable sign of mastoiditis in children. 

3. Occasional symptoms suggesting cerebral irritation,— e.g., convul¬ 
sions, sudden vomiting, chills, hyperpyrexia, etc., while naturally causing 
anxiety, are of less serious import than if occurring in an adult patient 
suffering from mastoid inflammation, for the reason that the cerebral 
centres presiding over these disturbances of function are more subject to 
reflex irritation from slight peripheral causes than in the adult. Such 
symptoms are not, however, even in very young children, to be consid¬ 
ered lightly, and the child exhibiting them should be very carefully watched. 

A conspicuous difference in the Physical signs of mastoiditis in early 
life depends upon the fact that the outer wall of the antrum in infants, 
and the outer mastoid cortex in children of two or three years, are softer, 
more vascular and spongy, and infinitely thinner than in later life. As a 
result of these structural peculiarities, perforation of the cortex with 
consequent subperiosteal abscess is a comparatively frequent and early 
manifestation of mastoid disease in early life.’ As a matter of fact, the 
diagnosis of mastoiditis in young children is frequently not made until 
after the appearance of postauricular oedema or subperiosteal abscess. 

Prognosis. —-Most cases of acute mastoiditis which are brought undei 
the care of a competent aurist recover without operation upon the mastoid. 
Of the minority which do not respond to non-operative measures, but which 
present no evidences of intracranial complications, the prognosis as to 
recovery after operation is very favorable. Taking any large series of such 
cases operated upon by competent aural surgeons, the percentage of 
mortality probably does not exceed 1 or 2 per cent. In those cases in 
which, either before or after operation, the intracranial structures become 
involved (brain abscess, meningitis, sinus thrombosis), the mortality is 
exceedingly large,— depending in part upon the character of the lesion, 
and in part upon the amount of surgical skill and judgment which are 

brought to their care. 



190 ACUTE DISEASES OF MIDDLE EAR AND MASTOID 

Treatment. —The patient should be ordered to bed, and kept there 
until all physical signs of mastoid inflammation have subsided. An active 
cathartic should be administered. During the first day or two, he should 
be given a liquid or very light diet. 

Early Myringotomy .—Irrespective of a previous incision of the drum 
membrane, it should again be incised under nitrous oxide anaesthesia, 
unless tympanic drainage is obviously adequate. I he ear should be 
irrigated with boric acid solution at regular intervals, the frequency of the 
irrigations being regulated in accordance with the amount of the discharge. 
A ball of sterile absorbent cotton may, however, be placed lightly in the 
concha to protect the ear from fresh infection from without, this being 
changed as often as it becomes saturated with pus. 

Application of Cold to the Mastoid .—If the surgeon believes the inflam¬ 
matory process to be in the incipient stage, the application of an ice-bag 
or of Leiter’s coil may be of positive value in retarding, and perhaps abort¬ 
ing, the attack. It should be used not longer than twenty-four hours 
and once removed should not be reapplied. After the stage of fluid pus 
formation is reached, it may reduce the vitality of the part of the degree 
actually favoring bone necrosis. 

The application of leeches to the mastoid, scarification, and blood¬ 
letting by means of the so-called “artificial leech, ” and the old practice of 
blistering the mastoid, while mentioned in some text-books, are practically 
without value, and are to be condemned as likely to produce a local sen¬ 
sitiveness to pressure which might obscure an important physical sign,— 
i.e., either increase or diminution of true bone tenderness. 

The administration of opium in acute mastoiditis is particularly inad¬ 
visable, for it may not only mask important symptoms, but, if repeated, 
soon reduces the patient to a condition of nervous irritability unfitting him 
for anaesthesia and surgical intervention, should these later become necessary. 

The successful non-operative treatment of acute mastoiditis depends 
largely upon the maintenance of free drainage from the vault until the 
processes of repair within the mastoid are established. If, therefore, 
during this critical period evidences of premature closure of the postero- 
superior quandrant of the drum membrane arise, there should be no hesi¬ 
tation or loss of time in re-incising it. The writer has seen many cases in 
which this simpler surgical measure has saved the patient from the major 
operation upon the mastoid. 

As to the criteria by which the results of non-operative treatment are 
to be judged, it is best to avoid dogmatism. The patient should, of course, 
be seen and examined carefully each day. If at the end of three or four 
days the discharge is less profuse and mastoid tenderness less marked, I 
should regard these conditions—fever, of course, being absent—as dis¬ 
tinctly favorable, and should these conditions show further improvement 
at the end of a week, I should look upon recovery without operation as 
probable. On the other hand, if a week passed without improvement in 
the patient’s condition, and particularly if mastoid tenderness remained 


INDICATIONS FOR MASTOIDECTOMY 


191 


unchanged or had become more pronounced, I should feel that the patient’s 
safety called for operative intervention. 

The indications for operating in acute mastoiditis may be summed up 
somewhat as follows: 

1. The development during acute mastoid disease of auricular dis¬ 
placement as a result either of postauricular oedema or subperiosteal 
abscess,—furunculosis of the canal being eliminated as a possible cause. 

2. The development during acute purulent otitis media of symptoms of 
vestibular irritation— e.g., vestibular nystagmus, vertigo, etc. calls for 
prompt opening of the mastoid in order to relieve the vestibular walls of 

the pressure or presence of confined pus. 

3. Marked tenderness on pressure, extending well beyond the limits of 
the antrum, and showing no tendency to diminution within five or six 
days following the incision of the drum membrane, would point to an 
active inflammatory process within the mastoid cells, calling foi suigical 
intervention. 

4. Marked variation in the quantity of pus discharged, its maximum 
flow being apparently too great to be explained by the tympanic lesion, 
its periods of diminution being coincident with the development of mastoid 
pain or tenderness (or both). Such a combination of symptoms consti¬ 
tutes one of the most positive indications for opening the mastoid. 

5. Mastoid symptoms having been present and having disappeared, 
a discharge from the tympanic vault which resists all rational non-opera¬ 
tive measures may, by reason of its persistence, justify the hypothesis of a 
necrotic area beyond the limits of the antrotympanic cavity. In such 
cases an operation is often the only means of saving the integrity of the 
organ and preventing serious impairment of function. 

6. Finally, evidences of mastoid disease having been present, the 
development at any time during convalescence of symptoms of septic 
absorption— e.g., chills, sweats, septic temperature, etc—would, in the 
absence of other concurrent disease, constitute a positive indication for 

immediate operation. . . 

In speaking of the above as positive indications for opening the mastoid, 

it must be understood that we are speaking from the view-point ol the 
patient’s safetywith the view of correcting a lesion which has be¬ 
come dangerous before danger signals proclaim that his life is already in 
jeopardy. Every aurist has seen cases of mastoid suppuration of t le 
severest type, in which operation seemed clearly indicated, recover without 
operation. He has also, however, seen patients by whom operation was 
delayed or rejected, return later with symptoms of intracranial infection. 
The aural surgeon is, therefore, frequently confronted with a grave respon¬ 
sibility If he waits in all cases until symptoms are present rendering 
surgical intervention absolutely obligatory, he will frequently find when 
■ these symptoms appear, that the question is shifted from the advisability of 
opening the mastoid to a far more serious one,— i.e the possibility of 
saving the patient’s life by any means at his command. 


CHAPTER VIII. 

CHRONIC MIDDLE-EAR SUPPURATION. 

Otitis Media Purulenta Chronica .—This term is applied to any tym¬ 
panic inflammation giving rise to a perforation of the drum-head which 
shows no tendency to heal and through which there is a more or less 
constant flow of pus. 

Etiology. —Probably every case of chronic purulent otitis media has 
its origin in one or more attacks of acute tympanic disease. As a rule, 
however, these patients apply for relief only after months or years of 
constant or intermittent otorrhoea, so that the early changes marking the 
conversion of the acute into the chronic form of the disease rarely come 
under actual observation. 

All observers who have had an opportunity of watching the ear changes 
in any large series of cases of the acute exanthemata must have been 
impressed with the remarkable rapidity with which the drum membrane 
is frequently destroyed in acute tympanic lesions complicating scarlet 
fever and diphtheria. In some cases this tendency is so pronounced that 
nothing the physician may do seems to exert the slightest influence upon 
the rapid and permanent destruction of tissue. Measles and influenza 
also contribute their quota to the number of cases of acute tympanic 
disease which ultimately become chronic. Probably from 18 to 20 per 
cent, of all cases of chronic middle-ear suppuration are traceable to the 
infectious diseases of childhood. 

Adenoids predispose the child so markedly to acute middle-ear disease 
and interfere so effectively with spontaneous recovery that they must be 
included among the active causes of chronic purulent otitis media. This 
explains in some degree the greater frequency with which the disease 
develops in childhood as compared with adult life. 

An occasional cause of the disease in adult life is found in the atrophic 
changes in the drum membrane occurring in some cases of non-suppurative 
middle-ear catarrh. The drum membrane in such cases may be exceed¬ 
ingly thin, transparent, and retracted, or may be apparently thickened and 
relaxed. Probably most aurists have seen cases in which, during an attack 
of acute purulent otitis media of apparently moderate severity, the mem- 
brana tensa has undergone rapid disintegration about the site of the perfor¬ 
ation, which has subsequently shown little tendency to regeneration. The 
rapid loss of tissue in these cases is probably due to atrophy of the normal 
fibrous layers of the membrana tensa, which are ordinarily so strongly resist¬ 
ant to the influence of an acute suppurative process within the tympanum. 

Giving due weight and consideration to other causes, there can be little 
doubt that the great majority of cases are directly traceable to neglect or un¬ 
skilful management of an antecedent attack of acute purulent otitis media. 

Pathology. —The drum membrane is necessarily perforated in every 
192 


MARGINAL PERFORATION OF DRUM-HEAD 


193 


case of chronic purulent otitis media. In the great majority of cases the 
perforation is central,— i.e., does not at any point involve the marginal 
attachment to the annulus tympanicus. In size it may vary from a minute 
pin-point orifice to practical destruction of the greater portion of the mem- 
brana tensa. It may also vary in shape from a small circular or oval 
opening to the larger crescentic or horseshoe-shaped defects involving 
both anterior and posterior segments. When the membrane bordering 
the perforation is relaxed and indrawn, and the tympanic mucosa is swol¬ 
len and denuded of its surface layer of epithelium, adhesions may form 
between the margins of the perforation and the inner tympanic wall. 

Perforation of ShrapnelPs membrane seldom or never occurs during 
acute purulent otitis media, but is found in about 3 per cent, of cases of 
chronic middle-ear suppuration (Bezold). While an artificial opening in 
ShrapnelPs membrane would lead into Prussak’s space, that occurring in 
chronic purulent otitis media invariably forms a direct communication 
with the vault, and therefore with the aditus and antrum. 

Marginal perforations—meaning thereby perforations in which there is 
at some point absolute destruction of the peripheral edge—are found in a cer¬ 
tain proportion of cases of long-standing middle-ear suppuration. They also 
occur primarily in certain cases of very rapid destruction complicating pro¬ 
found systemic infection, notably in cases of scarlet fever or diphtheria of 
unusual severity. Generally speaking, a marginal perforation ot the drum 
membrane must be regarded as pointing to a more serious lesion of the tym¬ 
panum than a central perforation, for the following reasons: (1) in a large 
percentage of cases, a marginal perforation indicates necrotic changes in the 
bone adjacent to the perforation: (2) the great majority of marginal perfora¬ 
tions involve either Shrapnell’s membrane or the upper posterior margin of 
the membrana tensa, in either case leading directly into the vault, aditus,and 
antrum; and (3) a marginal perforation involving Shrapnell’s membrane or 
the posterosuperior segment of the membrana tensa, or both, constitutes the 
ideal condition for extension of the epidermis of the meatus into the antro- 
tympanic cavity. This leads in some cases to a proliferation of epithelial ele¬ 
ments within the antrum, and provides the most favorable nucleus for the sub¬ 
sequent formation of cholesteatomatous masses within that cavity. Accord¬ 
ing to the author’s experience, marginal perforations always mean osseous 
necrosis, the structures most commonly involved being the malleus and incus 
and the contiguous portions of the tympanic ring and Rivinian segment. 

The Mucosa .—The changes in the mucous membrane may vary in 
different cases from simple hyperaemia with infiltration of leucocytes to 
practical destruction. In the simplest form of the disease, the mucosa 
may be greatly swollen so as to encroach considerably upon the cavity of 
the atrium, yet may preserve intact its surface layer of ciliated epithelium. 
This condition may persist for long periods without actual destruction of 
tissue. In the severer forms the epithelial covering is lost over consider¬ 
able areas, in which situations granulations form and there is a marked 
tendency to adhesions with adjacent structures. 

13 


194 


CHRONIC MIDDLE-EAR SUPPURATION 


Bone Changes .—It is quite possible for a chronic purulent otitis media 
to exist for a considerable period without producing caries oi the bony 
structures of the tympanum. For example, erosion of the superficial 
epithelial layer of the mucosa ma} r be followed by the formation of firm 
granulations which protect the periosteum and underlying bone. When, 
however, the entire thickness of the tympanic lining membrane is at any 
point destroyed, the exposed bone, being deprived of its periosteal support, 
must depend chiefly upon its own arterial supply. Whether in such a case 
the denuded bone has been able to maintain its own nutrition, is usually 
indicated by the character of the granulations: e.g., fairly rapid formation of 
a covering of firm, apparently healthy granulations usually indicates normal 
repair, whereas the slow formation of loose, friable granulations, through 
which a probe passes without appreciable resistance to bare bone, commonly 
indicates bone caries. This process involving the bony capsule of the laby¬ 
rinth— e.g., the promontory or the outer wall of the horizontal semicircular 
canal—may be self-limited, the diseased layer of surface bone being thrown 
off in the pus in the form of minute sequestra, and the bone being grad¬ 
ually covered by healthy granulations; or the necrotic process may involve 
the entire thickness of the labyrinthine wall, giving rise to a suppurative 
labyrinthitis. The latter result occurs in 1 per cent, of all cases of suppura¬ 
tive otitis media (Hinsberg). Destruction of the mucous membrane lining 
the vault, aditus, or antrum leads usually to a more destructive form of os¬ 
seous disease, from which spontaneous local recovery is comparatively rare. 

In the cellular bone surrounding the bony capsule of the labyrinth, 
and in that bounding the aditus and antrum, the disease in many cases 
involves a dual process, osseous necrosis or softening being apparently 
accompanied, or closely followed, by a proliferative osteitis, in consequence 
of which the diploic or pneumatic bone substance is ultimately replaced by 
very hard, compact bone. As a result of an extension of this process, 
the mastoid cortex is often greatly thickened, and the cellular character of 
the bone to a very considerable extent lost. 

Much has been said as to the influence of this pathological osteosclero¬ 
sis upon the gravity of the disease. Undoubtedly the marked increase in 
the thickness and density of the outer cortex renders an escape of pus 
through a perforation in this direction less likely to occur. On the other 
hand, it must be remembered that the process is not confined to the outer 
cortex, but occurs with equal regularity and frequency in the cellular bone 
surrounding the labyrinthine capsule, which it probably serves to protect. 
Bezold regarded it as a conservative process tending to limit the advance 
of a suppurative lesion in all directions. 

Granulations; Polypi .—Whenever in the tympanum there is actual ero¬ 
sion or destruction of tissue, however superficial, the process of repair is in¬ 
augurated by the formation of new granulations, which may later become 
organized into firm fibrous tissue. The presence of a certain amount of firm 
granulation tissue points, therefore, not so much to the disease itself, as to 
the effort on the part of the organism to repair or replace that which has been 



EPIDERMIZATION AND CHOLESTEATOMA 


195 


destroyed. On the other hand, the proliferation at certain points of loose, 
exuberant granulations, through which a probe at once passes to contact 
with rough denuded bone, is distinctly characteristic of osseous necrosis. 

Aural polypi may assume almost any shape within the limits of the 
tympanum and auditory meatus. They may be single or multiple; may 
consist simply of masses of granulation tissue, or may become partially 
organized, covered by squamous or ciliated epithelium, and assume some¬ 
what the character of fibromata. They may be attached by a compara¬ 
tively broad base or by a very small pedicle. They may spring from any 
denuded surface,— e.g., from the margins of a small perforation, from 
necrotic ossicles, from the promontory, or from the diseased tympanic 
margin, or tympanic ring. They are not infrequently attached to a denuded 
wall of the bony meatus near its tympanic margin. Very frequently they 
originate in the tympanic vault or the aditus. 

In the author’s experience, aural polypi point almost invariably to 
bone necrosis. While occasionally springing from the promontory, this 
site is exceedingly rare as compared with the outer wall of the vault or the 
diseased inner margin of the bony meatus. Aside from actual observa¬ 
tion and experience, the comparative rarity of polypi springing from the 
promontory may be inferred from the rarity of suppurative involvement of 
the labyrinth as compared with the frequency of polypi as a manifestation 
of chronic middle-ear suppuration. That is to say, if any considerable 
proportion of the polypi observed in chronic purulent otitis media had 
their origin from a diseased promontory, one would expect more frequent 
suppurative invasions of the labyrinth than are known to occur. 

Epidermization and Cholesteatoma. A noticeable change in certain 
cases of chronic purulent otitis media is the conversion of the tympanic 
mucosa into a grayish-white, non-secreting membrane bearing some 
resemblance to the skin of the meatus. It is seen oftenest in association 
with marginal perforations involving Shrapnell’s membrane and the upper 
posterior periphery of the membrana tensa. It may, however, occur with 
large central perforations. This so-called epidermization of the middle- 
ear cavity is inaugurated by extension of the epidermis of the meatus 
and drum membrane over the edges of the perforation and into the tym¬ 
panic cavity. This process, by converting the recesses ol the tympanum 
into dry cavities lined with a protective, non-secreting membrane, may be 
nature’s method of limiting the spread of the disease. There can be no 
doubt that in many cases spontaneous recovery has resulted from this 


process (Schwartze). 

Unfortunately, this happy sequence of events is not always realized. 
Let us imagine a case in which the epidermis of the canal, having entered 
the tympanum through a marginal perforation, extends by way ot the 
aditus to the walls of the antrum. The new lining membrane, perhaps 
becoming macerated by pus from a deep-seated focus of suppuration, is 
ultimately exfoliated, leaving, however, a similar epithelial layer beneath. 
Successive layers, being similarly thrown off, finally become welded m o a 


196 


CHRONIC MIDDLE-EAR SUPPURATION 


rather compact mass which can not be expelled through the aditus, and 
must inevitably increase in size. Such a mass has received the name 
of cholesteatoma. Examined under the microscope, it usually contains 
numerous pus germs, some cholesterin crystals, and quantities of epi¬ 
thelial cells. The outer surface usually preserves the arrangement of 
concentric epithelial layers, which are easily separable one from the other. 

The influence which cholesteatoma exerts upon the surrounding bone 
is one of gradual disintegration or absorption. The term absorption is in 
many cases more descriptive of the actual process than necrosis, since the 
latter destroys first the membranous lining or covering of the bone attacked. 
Cholesteatoma, on the other hand, may eat its way into contiguous bone, 
without the usual signs of suppuration, the enlarged and enlarging bone 
cavity retaining everywhere a well-defined epidermal covering. In such 
cases there may be little or no demonstrable discharge through the meatus, 
or there may be occasional very slight discharge consisting chiefly of the 
secretion from the newly-formed membrane mixed with decomposing epithe¬ 
lial cells. Such a discharge, when removed by means of a cotton-wound 
applicator, is usually unbearably offensive. In other cases the cholesteato- 
matous absorption of bone coexists, or rather alternates in different parts 
of the bone cavity, with the usual form of suppurative necrosis. The pus 
from such a lesion is often so indescribably offensive as to constitute in 
some degree a social barrier between the patient and his fellows. 

Illustrations of these two types of the disease are found in two cases 
operated upon by the writer. In one, a man over fifty years of age, the 
radical operation was performed on account of some of the more common¬ 
place symptoms of chronic middle-ear suppuration. On removing the 
cortex, the antrum, greatly enlarged, was found to contain a large choles- 
teatomatous mass, around which was a limited amount of secretion the 
stench of which was almost overpowering. In this case the operation was 
completed by the formation of a large meatal opening, and the patient 
made a perfect recovery. The second case was that of a strong Irish 
woman, a domestic, who suffered from a more or less constant discharge of 
so offensive a character that she found it difficult to retain any position 
longer than a few weeks. In this case cholesteatoma was found side by 
side with the usual signs of suppuration,— i.e., pus, granulation tissue, 
and necrotic bone in adjacent spaces. Removal of these products of dis¬ 
ease by the radical operation resulted in permanent cessation of the dis¬ 
charge. In both these cases, the evidence of progressive disintegration or 
absorption of bone rendered the danger of serious intracranial involve¬ 
ment, had surgical relief been withheld, very great. 

The serious nature of these cases depends upon a fact now fortunately 
recognized by all experienced otologists,—viz., that cholesteatoma con¬ 
fined in parts of the ear not accessible through the external auditory 
meatus, may lead to dangerous spread of the infection,— e.g., through the 
labyrinthine capsule, causing suppurative labyrinthitis; to the middle 
fossa of the skull, causing epidural or temporosphenoidal abscess; to the 


CHOLESTEATOMATOUS DESTRUCTION OF BONE 197 


posterior fossa, giving rise to infective sinus thrombosis or more rarely to 
cerebellar abscess. 

Before leaving this phase of the pathology, it may be admissible to 
mention certain very exceptional cases in which the cholesteatomatous 
mass has caused such extensive destruction of the posterosuperior wall of 
the bony canal as to accomplish practically the mechanical results of a 
radical operation. Probably most aurists have seen one or more such 
cases. The writer some years ago had referred to him a patient whose 
aural lesion presented the following interesting features: The patient, a 
man of fifty years, had suffered since boyhood from occasional discharge 
from his right ear. Inspection revealed such extensive destruction of the 
posterior wall of the bony meatus that it was not difficult to remove from 
the antrum through the canal an epithelial mass the combined bulk of 
which equalled that of a chestnut. The cavity from which this mass was 
removed was apparently lined throughout with an epidermal covering 
which could easily be reached through, the meatus. After removal of the 
growth, this patient was practically without aural symptoms up to the 



time of his death from pneumonia some years later. Bezold was among 
those who recognized this condition as one reasonably insuring the patient’s 
safety. The accompanying picture, drawn from a specimen in the writer’s 
collection, illustrates very nicely a stage of the process by which this 
mechanical result is reached (Fig. 115). 






198 


CHRONIC MIDDLE-EAR SUPPURATION 


Symptoms and Signs.— A suppurative process which by extension 
may reach the labyrinth, the brain cavity, or may infect the large venous 
channels of the brain, may obviously be the primary cause of many varied 
and complex phenomena. We shall limit our remarks, however, to a brief 
statement of the symptoms characterizing a suppurative lesion absolutely 
confined to the tympanum and adjoining mastoid cells. For the sake of 
brevity, it may be well to state in advance, that, aside from the discharge 
and the physical changes observed through the aural speculum, many 
patients endure this lesion for years without pronounced symptoms, 
either systemic or subjective. 

While it would seem reasonable to assume that a lesion capable of 
maintaining a more or less constant purulent discharge might also cause 
considerable systemic disturbance, it is a clinical fact that constitutional 
symptoms are in most cases absent. This fact is so universally recognized 
among aurists, that the development of constitutional symptoms e.g., 
fever, pulse changes, etc. —would suggest to an experienced observer 
either an intracranial complication or some unrelated intercurrent disease. 
This does not necessarily imply that a chronic suppurative otitis media 
may not in some cases react unfavorably upon the patient’s vitality, but 
simply that it rarely or never gives rise to characteristic symptoms of 
sepsis or of systemic disorder. The two symptoms of which these patients 
usually complain are the discharge and the impairment of hearing. 

The Discharge .—The aural discharge varies greatly in different cases of 
chronic middle-ear suppuration, and is of some diagnostic significance. 
In the first place, the discharge has in the great majority of cases a dis¬ 
tinctly offensive odor, whereas the discharge in acute purulent otitis media 
is usually odorless. It has been proved, however, that a mucopurulent 
secretion, unmixed with detritus resulting from necrotic bone or discarded 
epithelial elements, may be quite without odor. In certain neglected 
cases of chronic purulent otitis media, the exceedingly foul odor is due not 
so much to the tympanic changes as to the admixture with the tympanic 
secretion of decomposing epithelial cells from the diseased lining membrane 
of the bony canal. In such cases, measures applied to keeping the canal 
free of pus greatly modify the offensive character of the discharge. Chronic 
suppurative lesions characterized by deep-seated areas of bare and necrotic 
bone may give rise to moderate discharge of very offensive odor. In such 
cases, the secretion may be so limited in quantity that its odor becomes 
noticeable only when the aurist attempts to wipe out the tympanic cavity 
for purposes of examination. Finally there is a class of cases in which the 
foul character of the discharge may be a constant cause of discomfort and 
chagrin to the patient,— i.e., cases in which the aditus and antrum are 
filled with cholesteatomatous masses, decomposing particles of which are 
constantly being washed out in the aural discharge. In these cases the 
peculiarly offensive nature of the discharge, and the presence in it of choles- 
terin crystals and quantities of broken-down epithelial cells, are of con¬ 
siderable diagnostic importance in determining the character of the lesion. 


SYMPTOMS AND PHYSICAL SIGNS 


199 


Physically the discharge may be thick or exceedingly thin; profuse or may 
consist merely of a few drops of viscid secretion confined to the recesses of 
the tympanic cavity, the presence of which may be unknown to the patient. 
The frequent or occasional presence of blood in the discharge points, as a 
rule, to the presence of polypi or exuberant, vascular granulations. Micro¬ 
scopic examination of the discharge in cases of chronic purulent otitis 
media practically always shows a mixed infection. 

Deafness .—To some extent the hearing is impaired in almost every 
case of chronic suppurative otitis media. The functional loss depends on 
two conditions,—viz. (a) the partial or complete destruction of the mem- 
brana tensa and elimination of the malleus and incus from the function oi 
sound transmission; and (b) hyperplastic changes in the region of the oval 
window interfering with the mobility of the stapes. Fortunately, complete 
loss of the drum membrane and also of the malleus and incus is by no means 
inconsistent with very good hearing,— i.e., impairment so slight as to 
interfere but little or not at all with the patient’s enjoyment of life. On 
the other hand, the formation of organized fibrous bands binding the 
crura of the stapes to the niche of the oval window may cause very dis¬ 
abling deafness. It is not always possible to determine the presence or 
extent of these hyperplastic changes by inspection alone. Thus, in two 
cases with extensive destruction of the membrana tensa and practical 
disarticulation of the ossicular chain by necrosis of the long arm of the 
incus, one patient may exhibit remarkable acuteness of hearing while the 
other may be exceedingly deaf. In each case the niche of the oval window 
may be filled with granulation tissue almost or quite hiding the stapes. In 
such contrasting cases, labyrinthine disease being excluded, we can explain 
the deafness of one patient as compared with the auditory acuteness of the 
other only bv assuming that with the former fibrous adhesions between the 
stapes and the oval niche or window have taken place, while in the case of 
the latter the stapes is surrounded and covered by a mass of unorganized 
granulation tissue which acts vicariously with the stapes in the collection 
and transmission of sound waves from without. This hypothesis receives 
support from the numerous cases of chronic suppurative otitis media with 
retention of good hearing in which the hearing power has failed after spon¬ 
taneous recovery and epidermization of the inner wall of the tympanum. 

It is worthy of note that the deafness due to fibrous ankylosis of the 
stapes resulting from chronic middle-ear suppuration is regarded by Polit- 
zer as the type of deafness most amenable to treatment by surgical means, 
_ e ^ by division of adhesive bands passing between the head and crura of 

the stapes and the walls of the oval niche. . . 

The impairment of hearing in these cases is of the type generally 
characterizing lesions of the sound-conducting mechanism. In those cases 
showing large perforations or practical destruction of the membrana tensa, 
the perception of the lower musical tones is always very considerably 
reduced. This is in accordance with the investigations of Helmholtz, cor¬ 
roborated by Bezold and others, which showed that the drum membrane is 


200 


CHRONIC MIDDLE-EAR SUPPURATION 


particularly essential to the transmission of low musical tones. The middle 
and upper register may on the other hand be heard with apparently normal 
acuteness. In testing cases in which the sound waves were transmitted 
wholly by the stapes acting alone, the writer has met with a few instances 
in which there seemed to be some byperacusis for the very high tones of the 
scale,— e.g., the whistle. Hearing by bone conduction is regularly increased. 

Physical Signs .—On attempting to inspect the ear by reflected light, 
the depths of the canal— i.e., drum membrane or exposed inner wall of the 
tympanum—may be hidden from view by inflammatory products filling 
the auditory meatus. The canal may contain pus, detritus formed of pus 
mixed with exfoliated and decomposing epithelium, or may be occupied by 
a polyp partially or completely obstructing its lumen. The pus and epi¬ 
thelial debris are, of course, easily removed by the syringe or may be wiped 
out by means of a cotton-wound applicator. The removal of an aural 
polyp is not so simple a matter. 

Large aural polypi— i.e., polypi which nearly or completely fill the 
canal—are usually easily recognized at a glance. On the other hand, a 
small polyp, occupying the tympanic space or confined to the inner ex¬ 
tremity of the bony meatus, may be somewhat puzzling to the student or 
beginner: he may find some difficulty in determining whether such a 
growth is a polyp, a swollen inner tympanic wall, or a bulging and raw, or 
denuded, drum membrane. 

Diagnosis. —An aural polyp, large or small, presents the following 
physical characteristics: (1) It usually appears, as in most cases it is, 
nearer the orifice of the meatus, and therefore nearer the eye of the exam¬ 
iner, than either the bulging drum or the swollen tympanic mucosa. (2) 
It presents a raw and granular surface, usually easily distinguishable from 
the denuded drum membrane on the one hand and the swollen but intact 
tympanic mucosa on the other. (3) It is comparatively insensitive to 
palpation by the tympanic probe, provided the probe does not touch the 
canal wall, whereas the drum membrane and tympanic mucosa are ex¬ 
tremely sensitive to pressure. (4) It is usually freely movable in the canal. 
(5) The probe, carried beyond the polyp, may be passed in all directions 
around it, except where it is attached to the wall of the bony meatus or to 
the tympanic ring, at which point the probe will be arrested. If the polyp 
is attached to some point on the inner wall of the atrium,—the prom¬ 
ontory (rare), the probe will pass completely around it in either direc¬ 
tion. In these manipulations great care must be observed to avoid bruising 
the polyp, or free hemorrhage is likely to occur, making further examina¬ 
tion for the time being difficult or impossible. The question of removing 
the polypi through the canal, either for therapeutic purposes or to facilitate 
further examination, will be spoken of in connection with the treatment of 
chronic middle-ear suppuration. 

The auditory canal being free of pus or other foreign matter, one is 
able to determine the position and size of the perforation. Only rarely 
is the drum membrane completely destroyed, the tough peripheral edge 


CENTRAL PERFORATIONS OF DRUM MEMBRANE 201 


(annulus tenclinosus) being very resistant to suppurative disintegration. 
The majority of perforations are central apertures confined to the mem- 
brana tensa. They occur most frequently in the posterior segment (Figs. 
116 and 117), but are also found in the anterior segment (Fig. 118). With 
large perforations of the anterior segment, the posterior margin, drawn 
inward by the hammer handle, is often adherent at the level of the umbo 
to the promontory (Fig. 119). Perforations involving both anterior and 



Fig. 116. 




Fig. 119. 


Fig. 122. 



Fig. 117. 



Fig. 120. 



Fig. 123. 

Central perforations. 



Fig. 118. 



Fig. 121. 



Fig. 124. 


posterior segments are not uncommon, and are seen chiefly in three forms, 
apparently representing different stages of the destructive process: viz., 
(a) the kidney-shaped perforation confined to the lower part of the mem- 
brana tensa (Fig. 120); (b) the horseshoe-shaped perforation involving 
large central portions of both anterior and posterior segments, the manu¬ 
brium mallei remaining approximately intact (Fig. 121); and (c) the large 
irregularly heart-shaped perforation which is so often seen in cases of long¬ 
standing suppuration in which the hammer handle has been to a great 

























202 


CHRONIC MIDDLE-EAR SUPPURATION 


extent destroyed by the necrotic process (Fig. 122). All of the above 
examples fall under the head of central perforation when the peripheral 
edge is not at any point destroyed. 

There is usually no great difficulty in mapping out the boundaries or 
limits of a central perforation so long as the surrounding surface of drum 
membrane is covered by normal or at least recognizable epidermis. The 
margins of a perforation of long standing are commonly thickened and 
easily distinguishable from the tympanic surface beyond. 

A condition which is sometimes difficult to interpret correctly is found 
in cases in which the membrana tensa is not only perforated but also 
denuded of its epidermal covering, its outer surface being everywhere 
covered with fine granulations. When with this condition the mucosa 
covering the inner tympanic wall is swollen, granular, and crowded against 
the margins of the perforation, even the most experienced aurist may be 
unable to gauge correctly the extent of the injury until the remaining 
portion of the drum membrane has been restored by treatment to an 
approximately normal condition (Fig. 123). 

The inner tympanic wall seen beyond the margins of a large central 
perforation may have the appearance of fairly normal mucous membrane, 
or may be so swollen that the normal elevations and depressions are to a 
great extent obliterated. Or, again, the mucosa may for the most part be 
replaced by granulation tissue (Fig. 124). 

In some cases the lining membrane appears as a grayish-white, com¬ 
paratively dry membrane having some resemblance to the skin of the canal. 
This change in the tympanic lining is brought about in part by the in¬ 
growth through the perforation of the epidermal covering of the drum¬ 
head, and in part also by the action of the air upon the tympanic mucosa 
after the suppurative process as such has run its course. By this process, 
which is usually spoken of as epidermization, spontaneous recovery is 
brought about in certain cases. 

Marginal Perforations .—It is clear that any central perforation, by 
extension of the destructive process, may be converted into a marginal 
perforation. The commonest and most characteristic marginal perfora¬ 
tions are those in which the peripheral edge of the upper posterior segment 
of the membrana tensa and the adjacent part of Shrapnell’s membrane 
are destroyed, leaving bare the bony ring to which they were attached 
(Fig. 125). In the majority of such cases, according to my experience, 
the adjacent portion of the bony frame is also diseased and very fre¬ 
quently to some extent destroyed. Thus, through a marginal perforation 
including and extending somewhat behind Shrapnell’s membrane, one is 
occasionally able to see a considerable portion of the head of the malleus 
and body of the incus. This invariably indicates destruction of the inner, 
or tympanic, margin of the roof of the bony meatus (Fig. 126). With 
marginal, as with central, perforations, the landmarks of the tympanum 
may be completely hidden by granulation tissue or polypi (Fig. 127). 

In marginal perforations exposing the normal structures of the vault,— 


PERFORATIONS OF SHRAPNELL’S MEMBRANE 


203 


e.g., head of malleus or body of incus, or both,—these bones and the ex¬ 
posed tympanic cavity are seen in some cases to be covered by a white and 
apparently dry skin-like membrane, d his condition has a different surgical 
significance according to the presence or absence of discharge. If there is, 
and for a considerable period has been, complete absence of discharge, it 
may represent the final stage of local resolution by the conversion of the 
vault recesses into dry skin-covered cavities (Fig. 

128). On the other hand, a constant or even occa¬ 
sional flow of offensive pus from the aditus may be 
due to a cholesteatomatous collection within the 
antrum constituting a constant menace to life 
through.its possible invasion of the labyrinth or 
intracranial cavity. 

Perforations of ShrapnelVs Membrane .—These 
little perforations seem pathologically and clini¬ 
cally to constitute a class by themselves. They 




Fig. 125. 


Fig. 126. 



Fig. 128. 



Fig. 127. 



Marginal perforations. 



Fig. 130. 



Fig. 131. 

Perforations of Shrapnell’s 
membrane. 


are seen chiefly in three situations—viz., immediately above the short 
process of the malleus (Fig. 129), above and a little in front of the short 
process (Fig. 130), and perforations extending backward through t 
posterior stria of Prussak (Fig. 131). While comparatively uncommon 
a considerable number of these minute perforations can be seen duru g 
the year in any large aural clinic. The membrana tensa may be intact 
and apparently normal. Discharge from the vault may be fairly abundu 
exceedingly slight, or wholly absent. Discharge being absent, there may 





















204 


CHRONIC MIDDLE-EAR SUPPURATION 


be a history of past tympanic suppuration. Quite frequently no such 
history is obtainable. 

The exact pathogenesis of this condition has been, and still is, a sub¬ 
ject of controversy. The statement of Dench 1 that “a perforation above 
the short process always means intratympanic caries, and usually indicates 
that the malleus is affected,” is incorrect and might lead to surgical error. 
The ossicles may be, and in some cases certainly are, necrotic, but in many 
cases observed by the writer they were not. 

Two facts must be taken into account in any attempt to determine the 
origin of these perforations, viz., (1) that they rarely occur during an acute 
middle-ear suppuration, and (2) their frequent presence in individuals whose 
ears present no evidences of tympanic suppuration either past or present. 

Bezold stated that he had looked diligently for years for such a per¬ 
foration occurring during acute suppurative otitis media, but had never 
seen one. He connected their origin etiologically with chronic obstruc¬ 
tive lesions of the Eustachian tube, as a result of which Shrapnell’s mem¬ 
brane is first retracted, then becomes markedly atrophic, and finally breaks 
down. This theory seems in part to have been held by Hartmann (quoted 
by Politzer), who stated that he had repeatedly observed the coincidence 
of a perforation of Shrapnell’s membrane and a membrana tensa intact 
but retracted and adherent to the inner tympanic wall. 

Politzer states that he has more than once seen the development of 
a perforation in Shrapnell’s membrane during chronic middle-ear catarrh. 
His theory is that the membrana flaccida is first drawn into the depres¬ 
sion above the processus brevis, where it subsequently breaks down under 
the influence of compression by epithelial masses, there accumulating from 
the skin of the auditory canal. 

One of the most interesting contributions to the study of these minute 
perforations is found in a paper by Professor Schmiegelow, 2 published as 
far back as 1891. In it he described the physical changes in certain cases 
of acute suppurative otitis media in which a perforation of Shrapnell’s 
membrane provided the only pathway for the escape of pus. Two of these 
cases recovered promptly under rational treatment, leaving, however, the 
perforation of Shrapnell’s membrane as a permanent result. There is 
obviously no reason why such a perforation should be regarded as pointing 
to ossicular necrosis. 

There are of course cases in which perforations of the membrana 
flaccida are clearly associated with ossicular necrosis. 

Returning to the symptoms of chronic middle-ear suppuration, we 
must repeat the statement that, aside from the discharge, the impair¬ 
ment of hearing, and the physical changes in the ear itself, these patients 
are often practically without symptoms. 

Pain is not usually present in chronic suppurative otitis media, except 
as betokening one or other of the following conditions,—viz., (a) retention 

a Dench: Diseases of the Ear, p. 399. 

2 Schmiegelow: Perforations of the Membrana Flaccida Shrapnelli, Arch, of Otologv 
vol. xx, No. 3, pp. 228-256. 





INTRACRANIAL COMPLICATIONS 205 

♦ 

of pus somewhere within the tympanic vault, aditus, or antrum; or (b) 
acute exacerbations of inflammation, usually involving the mastoid cells. 
As a rule, pus under pressure quickly finds a pathway of escape, with 
prompt relief of pain. 

Many cases exhibit periodic variations in the amount of discharge, 
these changes being influenced by changes in the weather and other con¬ 
ditions causing nasopharyngeal congestion or inflammation. 

Acute exacerbations, accompanied by mastoid tenderness, are always 
to be regarded seriously in cases of long-standing middle-ear suppuration, 
for the reason that an acute inflammatory process confined within bone 
spaces, which may have been the seat of extensive previous disease, may 
naturally be separated only by thin barriers from vitally important intra¬ 
cranial structures. 

The course of the disease is very slowly progressive, and seems in many 
cases to be in some degree self-limited. That is to say, either by the pro¬ 
cess of osteosclerosis (eburnation) or by the formation of resisting walls of 
granulation tissue, the disease is in many cases confined during the major 
part of the patient’s life to the antrotyrnpanic cavity. This fact should be 
considered in its relation to the necessity for operative intervention. It 
does not, however, relieve the patient of the possibility of intracranial 
complication, which may ultimately occur in any case of chronic purulent 
otitis media. 

Complications. —The complications of chronic purulent otitis media 
may be mentioned in the following order: 

(a) Suppurative labyrinthitis, usually diffuse, rarely remaining cir¬ 
cumscribed. 

(b) Cerebellar abscess, infection very frequently by way of the labyrinth. 

(c) Cerebral abscess. 

(d) Meningitis, most often accompanying some suppurative lesion of 
the brain. 

(e) Infection of the sigmoid (lateral) sinus. 

There is no longer any doubt, that, in a very large percentage of cases 
of intracranial disease of otitic origin, the infection of the brain or men¬ 
inges is secondary to suppurative labyrinthitis. That this relation has 
not been more commonly recognized is due to the fact that the phenomena 
of labyrinthine disease have only recently received adequate recognition. 
Undoubtedly many cases of intracranial suppuration have been operated 
upon, and ended fatally, without any suspicion on the part of the medical 
attendants of a pre-existing suppurative labyrinthitis. 

Treatment. —The treatment of chronic purulent otitis media con¬ 
sists essentially of local treatment of the various morbid changes present, 
and in no disease do the physical changes vary so widely. Polypi, if 
present, must be removed, either through the canal or by radical opera¬ 
tion; ossicles, if to a certain extent diseased, must be removed; cholestea¬ 
toma must be dealt with radically. The ear should be irrigated in some 
cases, whereas in others irrigation is contra-indicated. Finally, there are 
certain cases which, in the author’s opinion, call for little treatment other 


20G 


CHRONIC MIDDLE-EAR SUPPURATION 


than certain simple measures for cleansing the ear, in which the patient 
should be instructed. Obviously no routine method of treatment can 
properly be described for this disease, hor example, routine iirigation of 
the ears with antiseptic solutions does not assure surgical cleanliness and 
rarely results in recovery. Clearly we must classify our cases before we 
can suggest rational lines of treatment. 

I. Let us consider first the simplest form of the disease,—viz., a case 
of comparatively short duration,— i.e., not over one or two years, and 
presenting the following conditions: central perforation of small or medium 
size which refuses to heal; discharge persistent but moderate in amount 
and free from the offensive odor characteristic of bone necrosis. Such a 
lesion falls under the head of chronic purulent otitis media when it has 
passed the stage in which spontaneous recovery may be hoped for. 

In searching for the chief obstacle to local recovery in a case of this 
character, we may find it in one or other of the following conditions: (a) 
In the first place, the mere presence of a small perforation subjects the 
middle ear to constant reinfection from the nasopharynx. With an intact 
drum membrane, occasional condensation of the air in the nasopharynx 
does not affect the tympanum further than to produce temporary increase 
of intratympanic pressure. With a perforation, on the other hand, every 
such condensation, as when the patient sneezes or blows his nose, carries 
a stream of air, impregnated with the impurities of the nasopharynx, 
through the tympanum, (b) The epidermal covering of the drum mem¬ 
brane may have extended over the edges of the perforation, rendering its 
closure by cicatricial tissue no longer possible; and (c) the lower part of 
the tympanic cavity may contain residual pus which the perforation by 
reason of its position can not drain. Routine irrigation with any solution 
is without value in such cases, and not infrequently is distinctly injurious. 

Bone disease being excluded by the character of the discharge, the 
treatment should aim at protection of the tympanum by closure of the 
perforation. As an initial measure, the canal should be wiped free of pus 
and dried. The nose and nasopharynx should be spra}^ed with some mild 
cleansing solution, the ear carefully inflated per catheter, and the drum 
membrane reinspected. Ordinarily a certain amount of pus or mucus 
will have been blown out into the canal, giving some idea of the condition 
of the lower (h} r potympanic) space. The canal and drum membrane are 
again wiped out, swabbed with alcohol, and the canal lightly packed with 
a wick of sterile gauze. This is to remain in the canal until the patient is 
seen by the aurist on the following day. This treatment should be repeated 
for several consecutive days, when we shall have gained fairly accurate 
knowledge of the tympanic condition. If the discharge is very slight, so 
that the canal and wick are found practically clean at the daily dressing, 
we may proceed at once in our efforts to close the perforation. If, on the 
other hand, a considerable amount of secretion is discharged daily, it may 
be necessary to obtain better drainage by a free incision through the 
membrana tensa, after which the wick treatment is continued as before. 


TREATMENT 


207 


When the discharge is reduced to a minimum, it may be found that 
the perforation is gradually closing under the stimulation of the daily 
cleansing and inflation. If no tendency to closure is observed, it may be 
that this is prevented by epidermization of the edges of the perforation. 
To correct this the edge of the perforation should be very lightly cauter¬ 
ized. For this purpose trichloracetic acid is the best agent. It is applied 
in the following way: The drum membrane is cleansed and thoroughly 
dried. A fine-pointed cotton applicator is tightly wound with a minute 
amount of absorbent cotton, which is dipped in sterile water, the excess of 
which is removed by sterile gauze. The cotton-wound end of the applicator 
is then plunged into a bottle containing crystals of trichloracetic acid, and 
rotated several times. Any adherent crystals are removed. Under inspec¬ 
tion by reflected light, the edges of the perforation are very lightly touched 
with the applicator. The influence of the acid is seen at once in slight 
whitening of the edges. The perforation may then be closed by a disk of 
paper prepared as follows: A disk of thin paper is cut of a size to extend 
slightly beyond the edges of the perforation; this is soaked in 95 per cent, 
alcohol, and then carried to its position covering the perforation by means 
of tympanic forceps or on the point of a cotton-wound applicator. Such a 
disk, if properly applied, adheres closely to the drum membrane. If no 
inflammatory reaction results, it should be allowed to remain in position 
until carried outward to the canal wall by the outward growth of epidermis 
covering the membrana tensa. Quite frequently the perforation will be 
found greatly reduced in size or may be closed. This, by protecting the 
tympanic mucosa, may end the lesion as a .suppurative process. 

In some cases this treatment may have to be repeated several times 
before the perforation is closed. In still other cases it may be impossible 
to obtain complete closure of the perforation, the dry, cleansing treatment 
resulting, however, in cessation of discharge. While a perforation per¬ 
sists, however, the patient remains subject to recurrences through infec¬ 
tion from without, or from the air current from the nasopharynx. 

II. Large Central Perforations without Polypi or Excessive Production 
of Granulation Tissue—It will be remembered that a central perforation 
may mean destruction of the entire membrana tensa with the exception 
of the marginal or peripheral edge (annulus tendinosus). In this condition 
restoration of the drum membrane is no longer possible. 

Under this head I wish to refer briefly to a class of cases with which all 
aurists are probably familiar, but which have, as a rule, received scant 
attention in otological literature. The physical picture is somewhat as 
follows: There is extensive destruction of the membrana tensa and fre¬ 
quently also of the hammer handle, the remnant of which may be adherent 
to the promontory. The tympanic walls are covered with mucous mem¬ 
brane or a layer of firm granulation tissue which does not disguise the 
landmarks of the inner tympanic wall,— e.g., promontory, niche of round 
window, etc. (Figs. 117 and 122). Rough, denuded bone is nowhere 
demonstrable either by inspection or by the tympanic probe. 1 he dis- 


208 


CHRONIC MIDDLE-EAR SUPPURATION 


charge or tympanic secretion may be slight, or may appear abundant 
simply as a result of neglect. In the latter case rational cleansing treat¬ 
ment soon reduces its amount. There are no evidences of labyrinthine 
involvement. Hearing tests may demonstrate a very fair degree of hear¬ 
ing power, the patient being at no disadvantage in communicating with 
his fellows; or the hearing may of course show considerable impairment. 

How shall we interpret this condition for ourselves and to our patients? 
Personally I believe that it in many cases represents a suppurative process 
which has run its course, or at least has become stationary, having erected 
its own barriers, either in the condensation of the bone itself, or in the 
production of firm granulation tissue between the focus of disease and 
surrounding structures. 

So long as the tympanum is lined by mucous membrane or granula¬ 
tion tissue, there must of necessity be some secretion or discharge, though 
this may be very limited in amount. This discharge can be absolutely 
terminated only by converting the tympanic spaces into skin-lined cavi¬ 
ties. But we can not be sure that such epidermization may not result in 
very considerable reduction of the patient’s hearing power. Every aurist 
knows of cases in which this has occurred. 

The point I wish to make is this: We should not be slaves to the dogma, 
too often repeated in otological literature, that aural discharge is neces¬ 
sarily of itself a danger signal, or one which when persistent calls for 
operative intervention. If we can satisfy ourselves that the discharge is 
simply the logical product of exposed mucous membrane or healthy 
granulation tissue, and that there is no evidence of an active suppurative 
process involving the bone itself, we should not be too ready to interfere 
with nature’s method of conservation. 

Treatment .—In my experience, the condition just described is not, as a 
rule, improved by routine, frequent irrigations. If when first seen the 
canal and tympanum show the result of neglect in residual pus,—usually 
very offensive in odor,—this should be removed by means of sterile cotton 
on applicators. The canal should next be filled with hydrogen peroxide, 
which should be allowed to remain at least five minutes. The ear is then 
syringed with a warm solution of boric acid,'after which the canal is filled 
with 95 per cent, alcohol, which in turn is allowed to remain a few minutes. 
The alcohol, itself an efficient cleansing agent, by its quick evaporation 
leaves the canal comparatively dry. Finally the canal and tympanum 
are “dusted” with boric-acid powder, introduced by a powder-blower. 
The canal is lightly filled with sterile gauze or the concha filled with sterile 
cotton. The patient is instructed to return at regular stated intervals for 
observation, at first on consecutive days. This treatment has the un¬ 
doubted advantage of reducing the amount of the discharge. 

When, finalfy, the physician has through careful treatment reduced 
the amount of discharge to a minimum, the patient should be instructed 
in keeping the ear clean. Many cases do well on the following routine 
treatment: Regularly once a week, the patient is to cleanse the ear by the 


TREATMENT 


209 


method first described,—using first hydrogen peroxide, then thorough 
boric-acid irrigation, and lastly alcohol. Following this the ear is to be 
dried with sterile absorbent cotton. While out of doors, the ear should be 
protected by a bit of sterile cotton in the concha, but not introduced into 
the meatus. Once daily, preferably at night, the meatus should be filled 
with an alcoholic solution of boric acid (gr. xx ad oj), which is retained in 
the ear a few moments only. If the alcohol causes severe “burning,” it 
may be diluted with sterile water, half and half. Under this treatment 
many patients suffer little or no discomfort, and the lesion remains qui¬ 
escent or its character may finally be changed by epidermization of the 
tympanic cavity. In some cases the frequency of the irrigations may be 
reduced to once in ten days; in others its repetition every three or four 
days may be required. It should, however, be repeated no oftener than is 
necessary to free the canal and hypotympanic space of residual pus. 

It is, of course, not claimed that the treatment above outlined will 
prove successful in every case presenting the physical characteristics 
described. There are some cases, for example, in which the discharge, 
whether it be scant or profuse, is perpetuated by a diseased condition at 
the tympanic mouth of the Eustachian tube. The tubal lesion may con¬ 
sist of an area of superficial osseous necrosis easily within the reach of a • 



Fig. 132.—Yankauer’s Eustachian curette. 


curette through the meatus; or, again, one aspect of the tube may be 
denuded of its mucous lining while a persistent mucosa of the opposite 
wall prevents the fibrous closure of the tube which is the first step toward 
permanent cessation of the discharge. When it can be determined that the 
principal seat of disease is located here, thorough curettage of the tubal 
region may bring about a cure. The purpose should be not only to remove 
any small focus of necrotic bone, but absolutely to remove the mucosa 
from that portion of the canal curetted. Possibly the best method of 
accomplishing this end may be that proposed by Yankauer. This proced¬ 
ure is carried out by means of a specially devised curette in the following 
way: The tympanic cavity, including both atrium and vault, is very care¬ 
fully cleansed. The Eustachian canal is cocainized by means of a 10 per 
cent, solution of cocaine, carried through the tube first by a cotton-wound 
applicator and then introduced through the Eustachian catheter. I he 
tympanum and pharjuigeal end of the tube are also cocainized. The 
Eustachian curette (Fig. 132) presents a shaft so curved that it may be 
introduced through the meatus and tympanum into the tube as far as the 
isthmus or slightly beyond. The cutting part consists of a terminal disk 
attached centrally to the end of the shaft. When carried to its position 
in the tube at or just beyond the isthmus, the shaft is rotated slightly 
back and forth so that a circular cut through the mucous membrane is 
14 






























210 


CHRONIC MIDDLE-EAR SIJP PUR AT 


made. When the surgeon is satisfied that the mucosa is completely di¬ 
vided throughout the entire circumference of the canal, the instrument is 
sharply withdrawn, separating the mucosa from the bony canal, and in 
some cases bringing it out inverted into the tympanum. This in favorable 
cases induces the formation of healthy granulations and subsequent per¬ 
manent closure of the tube. When this result is obtained, discharge from 

the tube naturally ceases, and the tym¬ 
panum is no longer subjected to this 
source of reinfection. 

III. Aural Polypi and Granulations 
(Fig. 133).—Polypi occluding the audi¬ 
tory canal interfere not only with drain¬ 
age but also with any plan of treatment. 
Polypi must therefore be removed either 
through the canal or by more radical 
operation. The first step is the deter¬ 
mination of the point of attachment by 
means of the probe. 

Most polypi are attached to the tym¬ 
panic ring, the posterior wall of the bony 
meatus, or spring from some point in 
the aditus. In these situations, they 
can usually be removed either in part or 
whole by means of the snare or a sharp 
ring curette, the latter instrument be¬ 
ing carried beyond the polyp and pressed 
against the bone surface to which the 
pedicle is attached. Unfortunately, 
such removal is very often followed by rapid re-formation of the growth. 

As a comparatively rare condition, polypi of considerable size have 
been found depending from the edges of a small perforation in the drum 
membrane. In such a case, the careful use of the probe detects the sur¬ 
rounding membrana tensa. Removal of the polyp in such a case has re¬ 
sulted in a cure (Bezold). 

Polypi springing from the promontory or other part of the inner tym¬ 
panic wall are rare as compared with the marginal attachments above 
referred to, and also represent a more serious condition. It must be 
remembered that the appearance of a polyp springing from any bone 
surface invariably represents nature’s effort to limit a necrotic process at 
that point. The attempt to remove a polyp springing from the promon¬ 
tory or the region of the oval window through the external auditory canal 
may be mechanically successful, but may too easily give rise to a laby¬ 
rinthine fistula, and consequent suppurative labyrinthitis, to appeal to me 
as good surgery. I am inclined, therefore, to regard polypi attached to 
the inner tympanic wall—the labyrinth itself having escaped invasion— 
as valid and sufficient grounds for performing a radical operation. 



Fig. 133.—Aural polyp. 





TREATMENT 


211 


Polypi not being present, or having been removed, the landmarks of 
the tympanum may be obscured or hidden by exuberant granulations 
(Fig. 124). This condition may be largely the result of neglect, the probe 
finding everywhere beneath the granulations a firm bed of healthy tissue, 
or, in other words, an absence of bare, necrotic bone. In this case, careful 
cleansing treatment, with occasional judicious use of astringents,— e.g., 
nitrate of silver, preferably in the form of a bead fused upon the end of an 
applicator,—may soon bring about a healthier condition. I have seen 
cases, in which the granulations were apparently exuberant and the dis¬ 
charge exceedingly offensive, show marked and quick improvement as a 
result of the following plan of treatment: The ear having been cleansed 
by the usual method and dried, boric-acid powder in considerable quantity 
is introduced into the tympanum, not by a powder-blower, but by means of 
a spatula. With a probe or other blunt instrument, the powder is well 
distributed over the tympanic surface, a central space being made for a 
sterile gauze wick. The wick is packed rather firmly in the tympanic 
cavity and loosely in the meatus. It is a mistake to believe that boric 
acid thus used may act as a dangerous obstruction to the flow of pus. 
Some of the powder is apparently always absorbed, and pus escapes 
through or around the remainder and is taken up by the gauze wick. The 
action of boric-acid powder thus directly applied is usually to cleanse and 
deodorize the cavity of the tympanum, and also in many cases to cause 
noticeable shrinkage of the granulations. In other words, it is both dis¬ 
infectant and astringent. 

In other cases the probe quickly reveals a lesion of different character, 
—passing without sense of resistance through the granulations to bare, 
necrotic bone. In this condition I can see no safe method of treatment 
short of a radical operation. 

IV. Marginal Perforations .—In the great majority of cases marginal 
perforations are accompanied by evidences of bone necrosis. Nearly 
always the contiguous portion of the tympanic ring is diseased, and the 
tympanic end of the roof of the bony meatus is occasionally eroded to a 
very considerable extent. In the latter instance the tympanic vault 
may be open to inspection, and the head of the malleus or body of the incus 
brought into plain view (Fig. 126). When the posterosuperior canal wall 
is to a considerable degree destroyed, we are frequently able to introduce 
a bent tympanic probe backward and slightly upward into the aditus and 
antrum. This condition, while giving evidence of the destructive power 
of the lesion, frequently adds to the patient’s safety by providing free 
drainage from the antrum and upper mastoid cells. Another frequent 
site of osseous necrosis is found in the ossicular chain. Almost invariably 
with large marginal perforations involving both membrana tensa and mem- 
brana flaccida, the malleus and incus will be found diseased, they may be 
completely destroyed. The incus, from its position in relation to the 
aditus and antrum and from its poorer blood supply, is the most frequent 
victim of the necrotic process, the malleus coming next. The stapes, by 


212 


CHRONIC MIDDLE-EAR SUPPURATION 


some fortunate provision of nature,—probably its abundant blood supply 
through the annular ligament,—is only rarely involved. The writer recalls 
at least three cases, however, upon which he performed a radical operation, 
in which no vestige of any ossicle, malleus, incus, or stapes, was present. 
In two of the three cases the labyrinth was involved in the suppurative 
process; in one the labyrinth was not involved. 

The treatment indicated varies somewhat in accordance with the fol¬ 
lowing conditions,—viz., (A) The presence of bare necrotic bone, (B) 
evidence of pus retention in the vault, (C) necrosis of the head of the 
malleus and body of the incus, and (D) recurring polypi or exuberant 
granulations in the aditus and vault. 

A. Osseous necrosis is evidenced in some cases by the constant recur¬ 
rence of exuberant granulations at some point, in others merely by the 
presence of bare rough bone. The significance of an area of necrotic 
bone as a surgical indication varies with the region involved. Thus, in 
surface necrosis of the promontory or region of the oval window, the danger 
of labyrinthine fistula and suppurative labyrinthitis calls for surgical 
intervention. On the other hand, a large marginal perforation involving 
both membrana tensa and Shrapnell’s membrane, and causing destruc- 

- tion of the upper posterior segment of the bony ring, may, by providing 
free drainage from the vault, aditus, and antrum, render the condition 
much less dangerous (Fig. 134). When with this condition the promontory 
is not diseased, and the antro attic cavity is not occluded by polypi, a 
bent probe passing without resistance backward and upward into the 
aditus and antrum, it is usually possible to cleanse the whole antrotym- 
panic cavity by the measures already advocated in the treatment of large 
central perforations. Such a case—particularly if functional tests dem¬ 
onstrate fairly good hearing power—should, in my opinion, be subjected 
to careful and rather prolonged cleansing treatment before a radical opera¬ 
tion is decided upon. 

B. Another variety of the lesion, by no means uncommon, is one in 
which, with extensive destruction of the membrana tensa below the pos¬ 
terior fold, that portion above the posterior fold and also Shrapnell’s 
membrane remain intact. The lower margin of this remnant of membrane, 
being more or less indrawn and adherent to contiguous structures, gives 
rise to occasional pus retention within the vault (Fig. 135). These patients 
suffer from periodic attacks of earache,—during which antrum tenderness 
is usually demonstrable,—these acute symptoms being usually relieved 
only after a free flow of pus from the vault is re-established. 

I believe that this is one of the most dangerous forms of the disease. 
An incision through the bulging remnant of membrane, the knife being 
carried upward into the vault, relieves the pain of the acute attack, but 
does not provide against recurrences. When operated upon radically, 
the aditus and antrum, and frequently the mastoid cells, are found to be 
extensively diseased. In the writer’s opinion, these cases represent the 
type of lesion in which extension of the suppurative process to intracranial 


TREATMENT 


213 


structures is most likely ultimately to occur. The safest treatment lies, 
therefore, in surgical intervention,— i.e., the radical operation. 

C. A r ecrosis of the Malleus and Incus .—Necrosis of the bodies of the 
malleus and incus is usually accompanied by the presence of surrounding 
polypi or exuberant granulations. The ossicles themselves may, there¬ 
fore, be hidden from view, even when the attic is exposed by erosion of the 
tympanic end of the roof of the bony meatus. The ossicles may be only 
slightly eroded or may be to a very great extent destroyed. In this con¬ 
dition granulations springing from the diseased ossicles, and also from the 
adjacent walls of the attic and aditus, may interfere very seriously with 
drainage of pus from the antrum (Fig. 136). 



Fia. 134. 


Fxa. 135 




Fig. 136. 



Fig. 137. 


Perforations of long standing. 


D. A somewhat kindred condition is that in which, evidences of ossic¬ 
ular necrosis being absent, the vault is filled with unhealthy granulations, 
apparently springing from the walls of the aditus (Fig. 137). 

The treatment of these conditions by any means short of surgical 
intervention requires patience and carries with it prolonged uncertainty 
as to whether an operation will not in the end become necessary. When 
the disease is perpetuated chiefly by ossicular necrosis, the logical means of 
relief would seem to be surgical,— i.e., either the removal of the ossicles 
through the auditory canal, or the more complete removal of all diseased 
structures by the radical operation. The relative value of these opera¬ 
tions will be referred to later. 

When the chief obstacle to drainage is found in polypi or exuberant 
granulations springing from the walls of the aditus, and a large marginal 














214 


CHRONIC MIDDLE-EAR SUPPURATION 


perforation brings this region into the practical reach of instruments, an 
attempt may be made to remove them through the canal, though I believe 
it is better surgery, and will prove in the majority of cases to the advantage 
of the patient, to proceed at once to the radical operation. 

Technic .—To begin with, the ear should be irrigated with bichloride 
of mercury solution (1 in 4000), and dried. A gauze wick, saturated with 
10 per cent, solution of cocaine, should be packed rather tightly against, 
and if practicable behind, the granulations and allowed to remain some 
ten minutes. We may then try to remove the granulations with a sharp 
curette. The ring of the curette should be carried in front of and beyond 
the granulations, and an effort made to remove them with one stroke of 
the instrument. With the cutting edge directed backward and outward 
against the inner surface of the tympanic ring, no damage can be done, 
whereas pressure of instruments inward against the inner tympanic wall 
is fraught with dangers outweighing in importance the advantages to be 
gained. Even after the use of cocaine, the first stroke of the curette is 
usually followed by free hemorrhage, interfering with the further exact 
use of instruments,—unless much time be allowed for repeated application 
of adrenalin, cocaine, etc. Enough may be removed, however, to provide 
drainage of the attic and spaces behind. Following this curettage, the 
wound is again irrigated, dried, and lightly packed with sterile gauze. For 
some days thereafter the patient should be seen daily. One of the best 
dressings in these cases is by a fairly thick covering of boric-acid powder, 
against which a wick of sterile gauze is lightly packed. This dressing 
should at first be changed daily, the ear being cleansed and dried each day 
before the wick is replaced. Under this treatment the tympanic condi¬ 
tion may change markedly and fairly rapidly for the better. When finally 
the use of wicks is discontinued, we should adopt as nearly as possible a 
dry method of treatment, frequent irrigation with warm solutions unques¬ 
tionably favoring the re-formation of redundant granulations. Should the 
granulations re-form within the aditus, it will usually be better to resort 
to the radical operation. 

V. Perforations of ShrapnelVs Membrane .—Perforations confined to 
Shrapnelbs membrane may for practical purposes be divided into two 
classes, viz., (1) those associated with a suppurative process within Prus- 
sak’s space, the tympanic vault, or even in the aditus or antrum beyond; 
and (2) those in which all signs of tympanic suppuration are absent. The 
writer personally believes that these small perforations without any evi¬ 
dences of present suppuration represent in many cases the result of a past 
infection of one of the membranous spaces of the vault; and further that 
such lesions, if circumscribed, may be credited with a certain tendency 
toward spontaneous resolution. This hypothesis seems justified by the 
number of such cases (Figs. 129, 130 and 131) in which, with a history of 
acute tympanic disease long since ended, discharge is absent or negligible, 
and the hearing but little or not at all impaired. These little perforations 
are in many cases so inconspicuous as to be easily overlooked unless 
systematic search is made for them. 


TREATMENT OF ATTIC SUPPURATION 


215 


When the discharge is continuous and profuse, one may be obliged to 
infer that the attic, and probably also the aditus and antrum beyond, 
are involved in the suppurative process. 

Treatment .—When the hearing is good and the discharge very slight, 
I am inclined to let these ears very much alone. Occasional irrigation by 
the physician himself by means of the attic syringe or cannula may be of 
value. I believe that this should be repeated only when there is evidence 
of pus collection behind the perforation. The use of alcohol, or alcoholic 
solution of boric acid, the canal being partly filled therewith once or twice 
daily, is of distinct value in some cases. 

When the discharge is so profuse as to constitute a proof of extensive 
suppurative involvement of the vault, surgical intervention may be called 
for. In this condition, I am inclined to believe that a radical operation is 
in many cases not indicated, and that a rational procedure, and one which 
does not endanger the hearing power, is by a simple mastoidectomy, the 
aditus being very carefully and thoroughly cleared of granulations and 
diseased bone. The aditus should be kept open until all evidences of attic 
suppuration have disappeared. I have used this method in a few cases of 
long-standing attic suppuration with very good results. 

Obviously there will be cases in which this operation will fail on account 
of necrotic changes requiring more radical treatment than a simple mas¬ 
toidectomy makes possible. When the simpler operation proves success¬ 
ful, the gain to the patient in the saving of drum membrane and ossicles 
and the preservation of function is very great. For this reason, the simpler 
operation is not only justified, but, in my opinion, indicated in cases in 
which it offers fair promise of success. The patient, however, should be fore¬ 
warned as to the possible necessity of later recourse to the radical operation. 

Cholesteatoma .—The presence of cholesteatoma within the antrum 
can not always be determined. In some cases, however, characteristic 
masses may be seen projecting into the vault from the aditus, and in others 
their presence may be inferred from the persistently offensive character of 
the discharge or the occasional presence therein of characteristic epithelial 
elements. Systematic examination of the discharge under the microscope 
for cholesterin crystals and broken-down epithelial cells would probably 
indicate its presence in many unsuspected cases. 

The treatment of cases in which the presence of cholesteatoma can be 
.determined may be summed up in three words ,—the radical operation. 
Such a growth, from its power of causing osseous disintegration or absorp¬ 
tion in any or all directions, constitutes a condition in which the patient is 
constantly exposed to the danger of intracranial infection. The operation 
in these cases should provide for an enlarged meatal opening through 
which all parts of the tympanomastoid cavity can be reached, and subse¬ 
quent cholesteatomatous collections prevented. 

Operative Indications .—From a descriptive viev'-point it is clear that 
“chronic purulent otitis media” is an elastic term covering a variety of 
conditions. While some of these constitute a positive menace to the life 


216 


CHRONIC MIDDLE-EAR SUPPURATION 


of the patient, in others the danger of intracranial invasion is exceedingly 
remote. The responsibility of the surgeon in the matter of his advice to the 
patient is, therefore, not small. If his duty in some cases is to state posi¬ 
tively his belief that the patient/s safety demands surgical intervention, 
there are others in which it is no less his duty to state with equal frank¬ 
ness his belief that operation is not required, and this without emphasis 
upon remote eventualities which the patient is not likely to experience. 

In this connection I am reminded of a remark of Professor Korner of 
Rostock, in watching whose work I had the privilege of spending a very 
instructive week some years ago. Upon my expressing the hope that I 
might see him perform a radical operation, he said: “Well, we may have 
to wait for the proper case. There are so many cases of chronic purulent 
otitis media, but so few in which the radical operation is really indicated.” 

The radical operation is an attempt at once to remove all diseased bone 
and to provide absolutely free drainage of all infected recesses of the antro- 
tympanic cavity by way of the external auditory meatus. 3 Many attempts 
have been made to formulate the indications for this procedure, resulting 
in some cases in lists of considerable length. In the writer’s opinion 
there are comparatively few conditions which can safely be given as positive 
indications for this operation. These may be mentioned somewhat in the 
following order: 

1. The persistent recurrence of exacerbations of acute inflammation 
accompanied by mastoid tenderness or pain and physical evidences of 
pus retention in the vault. In these cases we may assume that the antrum 
and mastoid cells are the seat of a subacute suppurative process, an advance 
of which may be recorded with each succeeding attack. I believe that these 
recurrent attacks indicate one of the most dangerous forms of the disease, 
and that they should be regarded as a positive indication for the radical 
operation. 

2. Evidences of fistula leading from the mastoid cells either through 
the posterior wall of the bony meatus or through the outer cortex. The 
latter condition gives rise either to marked postauricular oedema or to 
subperiosteal abscess. Mygind, 4 analyzing 100 cases of subperiosteal 
abscess treated in the Copenhagen Commune Hospital, observed 22 cases 
in which the cortical perforation resulted from an acute mastoid inflam¬ 
mation complicating chronic suppurative otitis media. In 16 of these 
cases (75 per cent.) the vault and mastoid cells were filled with choles¬ 
teatoma. This would apparently indicate that postauricular swelling 
points usually to a more serious condition in chronic middle-ear suppura¬ 
tion than in primary acute disease of the tympanum and mastoid. It is 
a positive indication for immediate surgical intervention. 

3. The dangers of cholesteatoma within the antrum or mastoid cells 
have already been explained. Hinsberg, Neumann, and others who have 

3 The radical operation is described in detail in the section devoted to Aural Surgery. 

4 Mygind: Subperiosteal Abscess of the Mastoid Region, Annals of Otoloev 1910 

pp. 529-540. * 





INDICATIONS FOR THE RADICAL OPERATION 


217 


studied the etiology of suppurative labyrinthitis, have found that a large 
percentage of cases are traceable to the action of cholesteatoma upon the 
bony capsule of the labyrinth. The determination of cholesteatoma is, 
therefore, a positive indication for the radical operation. 

4. Polypi springing from the promontory or region of the oval window 
can not be removed through the auditory meatus without great danger of 
producing a labyrinthine fistula. They are, therefore, an indication for 
a very careful radical operation. 

5. Persistently recurring polypi from any part of the tympanum— 
showing bone necrosis which non-operative treatment fails to eradicate— 
constitutes a logical reason for performing the radical operation. 

6. Very profuse and persistent discharge,—either by reason of the 
patient’s discomfort or the evidences it may afford of deep-seated bone 
disease, may constitute a valid reason for surgical intervention. 

7. Facial paresis or paralysis, occurring during the course of chronic 
middle-ear suppuration, evidences of suppurative labyrinthitis being 
absent, is a positive indication for very careful performance of the radical 
operation. 

If in the above list the author has omitted certain conditions usually 
included among the indications, he has done so with intention. For 
example, one writer, for whom the author entertains the greatest respect, 
includes “recurrent attacks of dizziness, nausea or headaches” occurring in 
chronic purulent otitis media as the operative indications. These symp¬ 
toms may or may not call for the radical operation. If due, for example, 
to suppurative labyrinthitis, the radical operation alone would be most 
positively contraindicated. This brings us to the consideration of a rule 
which all aural surgeons will do well to respect,—viz.: No patient should 
be subjected to the radical operation until his labyrinth has been carefully 
tested for evidences of suppurative labyrinthitis . 5 

Ossiculectomy. —Before leaving the subject of treatment, a word should 
be said of the operation of ossiculectomy. This operation proposes to 
provide freer drainage from the vault, aditus, and antrum by the removal 
of the diseased malleus and incus and incidentally of diseased remnants 
of the drum membrane which might interfere with the escape of pus from 
the vault. It is, therefore, in a way a substitute for the radical operation. 
If it were possible to determine that the diseased ossicles were the sole 
obstacles to resolution, or that their removal would insure resolutions 
in spite of infection within the mastoid cells, the arguments in favor 
of this procedure would have a more logical basis. I know, how¬ 
ever, of no positive indication for the selection of this operation, for the 
reason that there is no way of positively excluding deep-seated foci of 
bone disease which also might require surgical eradication. For this 
reason I have personally preferred the radical operation in all cases of 

5 The various tests for suppurative disease of the labvrinth are given in the chapter 
dealing with Suppurative Labyrinthitis. 



218 


CHRONIC MIDDLE-EAR SUPPURATION 


chronic purulent otitis media in which surgical intervention was deemed 
necessary. I can, however, conceive of many cases in which the slighter 
operation might prove successful, and in this event the advantages to the 
patient might be very considerable. 

The most favorable cases for the operation are those in which, with 
evidences of ossicular necrosis, there is no demonstrable exposure of bare 
bone in other directions, and in which the patient has retained good hear¬ 
ing power. 

In such a case I see no objection to this operation, the patient being 
made to understand that the results are somewhat uncertain and that in 
case ot failure a radical operation may later become necessary. 


CHAPTER IX. 


CHRONIC NON-SUPPURATIVE DISEASES OF THE MIDDLE EAR; 

OTOSCLEROSIS. 

Chronic catarrhal otitis media is an elastic term rather indefinitely 
applied to a variety of tympanic conditions not easily classified. There 
can be little doubt that many of the conditions resulting in impaired hear¬ 
ing, and described in text-books under different names as pathological 
entities, are in reality but different stages of a slowly progressive lesion. 
Our knowledge of these conditions is based very largely upon clinical 
study of cases, and observation of such morbid changes as can be seen in 
the living patient, and only to a limited extent upon actual study under 
the microscope of the tissue changes involved. It is clear, therefore, 
that, whatever classification may be adopted, the different groups will be 
found more or less to merge one into the other, and it is by no means im¬ 
possible that future investigation may show more definitely either their 
pathological relationship or independence. 

The chronic non-suppurative lesions of the ear may be considered 
under the following heads: 

1. Chronic tubal catarrh without marked tympanic changes other than 
those due to retraction of the drum membrane. 

2. Chronic catarrhal otitis media. 

3. Chronic hyperplastic otitis media; dry catarrh of the middle ear. 

4. Otosclerosis. 

CHRONIC TUBAL CATARRH. 

Obviously a catarrhal condition of the Eustachian tube may exist for a 
considerable period without producing ear symptoms. Only those cases, 
therefore, are likely to come under the otologist’s care in which the calibre 
of the tube is so reduced as to interfere with the passage of air to the 
tympanum. 

The causes of chronic tubal catarrh are exactly the same as those 
mentioned as predisposing factors to the acute type, and need not be re¬ 
peated here. In nearly every case will be found some condition either in 
the nose or nasopharynx interfering with nasal respiration. 

The history in characteristic cases is that of very moderate impair¬ 
ment of hearing characterized by periods of amelioration. The patient 
may tell you that there are considerable periods during which he is not 
conscious of any loss of auditory acuteness; or he may associate his periods 
of improvement with periodic changes of residence,— e.g., as related to 
vacation periods in the mountains or at the sea-shore. Usually the hear¬ 
ing is very considerably influenced by weather conditions, improving in 
dry clear weather and relapsing with the reverse conditions. With the 

219 


220 NON-SUPPUKATIVE DISEASES OF MIDDLE EAR 


impairment; of hearing, and often changing with its variations, tinnitus 
aurium is almost invariably present. Interrogation usually elicits the 
fact that the patient suffers at times from difficulty in nasal respira¬ 
tion, and physical evidences of some degree of nasal obstruction are 
usually present. 

Functional examination shows very moderate impairment of hearing 
of the general type characteristic of disease confined to the conducting 
apparatus,— e.g., slight loss of hearing for the lower musical tones and some 
increase in hearing by bone conduction. The ratio between hearing by 
air conduction and bone conduction is never reversed in a chronic lesion 
confined to the Eustachian canal. 

On physical examination the drum membrane is found to be retracted. 
In adults suffering from chronic tubal catarrh of not very long standing, 
the retraction may be of moderate grade, more pronounced displacement 
being at first opposed by the natural strength and resistance of the mem- 
brana tensa. Children, on the other hand, not infrequently exhibit with 
chronic tubal disease very extreme grades of retraction. 

A very characteristic feature of chronic tubal catarrh is found in the 
fact that the patient’s sense of functional loss or disturbance is frequently 
out of all proportion to any functional changes which may be demonstrated 
by the usual hearing tests. Conversational and whispered speech and the 
acoumeter may be heard at distances only moderately under the normal, 
and the change in the lower tone limit may be so slight as to leave one in 
doubt as to its significance. If the lesion be unilateral, however, there is 
a demonstrable difference— i.e., increase—in bone conduction in the in¬ 
volved ear. As compared with these rather negative findings, the patient 
himself is in no doubt as to his sense of diminished hearing power. I believe 
that a recognition of this seeming paradox or contradiction is extremely 
important, for otherwise we may believe, and assure the patient, that his 
auditory disturbance is transitory and of little importance, whereas 
his aural disorder is in reality at just that stage requiring most 
careful study and attention in order to avert changes leading to later 
serious functional loss. 

Another characteristic feature of this lesion is the very marked sub¬ 
jective sense of functional improvement resulting from inflation. The 
impairment, it must be remembered, is a mechanical one, due, in the early 
stages of the disease, not to pathologic changes within the middle ear. 
but to partial fixation of the membrane and ossicles by unopposed atmos¬ 
pheric pressure from without. If the impairment is slight, the hearing 
may be practically restored to the normal, and if of more advanced grade, 
the improvement resulting from a first inflation is very much more pro¬ 
nounced than that which occurs in chronic lesions of the tympanum. This 
point is, therefore, an important one both in the diagnosis and prognosis 
of these cases. 

Under chronic tubal catarrh, it may be admissible to recognize three 
conditions causing retraction of the drum membrane,—viz. (a) nasal 


CHRONIC TUBAL CATARRH 


221 


obstruction, the tube remaining patent; (b) tubal congestion; and (c) 
constriction clue to actual hypertrophy of the tubal mucosa. 

Nasal Obstruction.— I here are certain cases in which, as a result of an 
obstructive nasal lesion, the tubes remaining open, the air in the naso¬ 
pharynx is more or less rarefied with each inspiration. In consequence 
of this, the air-pressure within the tympanum becomes constantly negative, 
and retraction of the drum membranes and some impairment of hearing 
result. In such a case, inflation per catheter results in a fairly good current 
of air to the tympanum, replacement of the drum membrane, and prompt 
relief of the subjective symptoms. The relief thus afforded is, however, 
exceedingly short lived, the patency of the tubes conducing to the quick 
reduction of the tympanic air-pressure under the influence of the naso¬ 
pharyngeal lesion. Obviously, in such a case, no amount of local treat¬ 
ment of the ears by inflations, pneumatic massage, etc., will be of any 

permanent value until the nasal lesion, whatever its nature, has received 
attention. 

Chronic Tubal Congestion. —Belonging more properly to this group 
are those cases in which the tubal mucous membrane is the seat of chronic 
venous congestion. These patients present symptoms and physical signs 
almost identical with those just described. Inflation, however, gives 
unmistakable signs of obstruction due to congestion, the sounds through 
the diagnostic tube being at first muffled, rasping, or accompanied by moist 
rales, then becoming clearer as air enters the tympanum in greater volume. 
Inflation results in marked temporary relief of s 3 r mptoms, and the gradual 
improvement in the auscultatory signs resulting from repeated inflations 
shows more or less clearly that the lesion is chiefly one of chronic venous 
congestion. 

Another method of determining the character of the occlusion is by 
applying a 4 per cent, solution of cocaine by means of a bent cotton- 
wound applicator to the mouth and walls of the pharyngeal end of the 
tube. 1 Instead of cocaine, a 1 in 1000 solution of adrenalin may be used, 
but cocaine is preferable. If the action of the cocaine or adrenalin, thus 
applied, is exerted rapidly— i.e., in one or two minutes—throughout the 
canal so as to restore its lumen to a practically normal calibre, we may 
assume that the obstruction is due chiefly to venous congestion. On the 
other hand, if inflation, following this application, does not demonstrate 
a notable effect upon the calibre of the canal, we may assume that the 
lesion is one of structural thickening, inflammatory infiltration, or at least 
of tissue changes more complex or advanced than simple venous engorge¬ 
ment. If, finally, the application of cocaine or adrenalin exerts no appre¬ 
ciable influence upon the calibre of a constricted tube, we must infer ten¬ 
tatively that the lesion is one of cicatricial or hyperplastic narrowing or 
stenosis. This deduction must not, however, be accepted as conclusive 
until we have further investigated the tubal condition by means of a 

1 The cotton applicator for the local application of drugs to the pharyngeal end of 
the tube is described on page 152. 




222 NCN-SUPPURATIVE DISEASES OF MIDDLE EAR 


Eustachian bougie. It may be that the congestion or inflammation in the 
pharyngeal end of the tube or in the neighborhood of the isthmus is so 
great as to have limited the action of the cocaine strictly to the pharyngeal 
end of the tube, yet this localized obstruction may yield readily to the 
gentle passage of the bougie. Combining these methods it is usually 
possible to interpret correctly the nature of the tubal lesion. 

The importance of this careful preliminary investigation of the character 
of the tubal disease must be obvious to the reader, since it is clear that we 
can not determine upon a rational method of treatment until we know the 
character of the lesion which is to be the object of our attack. 

Treatment. — Cases of tubal venous congestion usually respond 
readily to rational treatment. This should include correction of any con¬ 
dition within the nose or nasopharynx which might act as an excitant of 
tubal congestion; application of astringents to the inflamed pharyngeal 
end of the tube; occasional catheter inflation for the purpose of restoring the 
membrana tensa to its normal position. 

For adult patients, inflation by catheter possesses among others the 
following advantages over the Politzer method: It enables one, by means 
of clearer otoscopic sounds obtained, to determine with greater accuracy 
the condition of the tube, and to measure the progressive improvement 
resulting from successive treatments. It eliminates the danger—where 
one ear only is diseased—of producing undue relaxation of the opposite 
drum membrane. With children, on the other hand, it is nearly always 
necessary to depend upon Politzerization. 

Many of these cases require no other treatment than the use of anti¬ 
septic sprays and the local application of astringent drugs, e.g., silver 
nitrate, argyrol, etc., to the naso-pharynx and pharyngeal ends of the 
Eustachian tubes. 

Structural Narrowing of the Tube— There is still another class of 
cases coming under the general head of tubal catarrh,—viz., cases in which 
the obstruction depends not merely upon venous congestion, but also to 
some extent upon actual increase in the normal tissue elements (h} r per- 
trophy). In more advanced cases the process may have given rise to a 
proliferation of new connective tissue (hyperplasia). The disease may occur 
as a uniform thickening of the tubal mucosa, or as localized deposits hav¬ 
ing a tendency to contract. During inflation the sounds through the oto¬ 
scope are insufficient, high-pitched or may be almost whistling in character, 
clearly indicating the reduced calibre of the tube. With such a lesion, we 
are justified in grouping under the general heading of chronic tubal catarrh 
only those cases of very moderate impairment of hearing which show 
sufficient improvement after inflation to exclude serious involvement of the 
tympanic structures. In.the great majority of cases, however, these pa¬ 
tients do not come under the observation of the otologist until evidences of 
organic disease within the tympanum are also well marked, i These 
advanced lesions of the tube will be considered in connection with the 
tympanic lesions to which they give rise. 


CHRONIC HYPERTROPHIC OTITIS MEDIA 


223 


CHRONIC NON-SUPPURATIVE TYMPANIC DISEASE. 

In attempting to describe the two main types of chronic middle-ear 
catarrh, yiz., chronic hypertrophic otitis medio, and chrome hyperplastic 
otitis media , or dry catarrh—it must be understood that they probably in 
most cases represent different stages of the same disease ; or, in other words, 
that one is sequel to the other. However this may be,— i.e., whether they 
in some cases represent the gradual conversion of a simple exudative 
inflammation into a hyperplastic condition in which the normal tissue 
elements are to a considerable extent replaced by new connective tissue, 
and in others originate independently as separate lesions from their incip- 
iency,—there can be no doubt that as seen by the aurist they occur as 
conditions having a different pathologic basis, and also differing substan¬ 
tially in their response to treatment. 

Chronic hypertrophic otitis media may be defined as a chronic exudative 
inflammation of the Eustachian tube and tympanum, whereby the lining 
membrane of both is greatly thickened and the calibre of the tube re¬ 
duced, with resulting impairment of hearing. 

Etiology. —Unfortunately, the lesion is frequently so advanced when 



of subacute catarrhal otitis media, in which resolution is never quite 
complete; (2) frequent attacks of acute rhinitis, each attack giving rise 
to more or less tubotympanic congestion; and (3) obstructive naso¬ 
pharyngeal lesions resulting in chronic tubal catarrh which later involves 
the tympanum. 

The influence of gout and rheumatism is clearly a factor in some 
cases of chronic middle-ear catarrh, and such a diathesis should be taken 
into account as suggesting certain lines of treatment which may be 
indicated. 

Pathology. — Pathologically this lesion is characterized by morbid 
changes within the Eustachian tube and also within the tympanum. The 
middle ear, as well as the Eustachian canal, is the seat of a subacute in¬ 
flammation involving primarily the mucous membrane. The character¬ 
istic changes are congestion and round-cell infiltration, leading later to the 
formation of a variable amount of new connective tissue. As a result of 
these changes, the mucous membrane everywhere throughout the tubo¬ 
tympanic space is greatly thickened. The calibre of the tube is there¬ 
fore considerably reduced, and may be practically closed to the auto¬ 
matic passage of air to the tympanum. Within the tympanic cavity 
the most pronounced changes, according to Politzer, occur in the 
neighborhood of the labyrinthine windows and in those situations where 
the ossicles are in contact with the tympanic walls. Diffuse inflam¬ 
matory thickening, then, is the earliest characteristic feature of this 


224 NON-SUPPURATIVE DISEASES OF MIDDLE EAR 


lesion. Naturally such changes can not fail to interfere with the mobility 
of the ossicles. 

In addition to the diffuse changes above described, there are occasion¬ 
ally developed certain secondary products of inflammation, instances of 
which have been seen and recorded by Toynbee, von Troltsch, Politzer, 
Moos, Bezold, Gradenigo, and others. These secondary changes usually 
take the form of adhesive bands between adjacent structures,— e.g., be¬ 
tween the crura of the stapes and the walls of the oval niche, between 
one or both arms of the stapes and the long arm of the incus, between the 
hammer handle and the promontory, or between adjacent surfaces 
of the ossicular joints. Contraction of these bands tends to limit still 
further the mobility of the ossicles. When adhesions occur between 
the hammer handle and promontory, the inward curvature of the mem- 
brana tensa is increased and the tensor tympani may be permanently 
shortened. 

Symptoms. — A consideration of the varied morbid changes which 
may occur in the course of this lesion makes clear to us the wide varia¬ 
tions in symptoms which different cases present. Usually the symptoms 
are very gradual in their development, so that the lesion may be well 
advanced before the patient applies for treatment. The first subjective 
symptom to attract his attention may be either impaired hearing or 
tinnitus aurium. 

Impairment of Hearing .—Deafness in chronic catarrhal otitis media is 
usually of very gradual development and never becomes complete,— i.e., 
unless disease of the auditory nerve or labyrinth is superadded to the tym¬ 
panic lesion. If the patient comes under the aurist’s care during the incip- 
iency of the disease, the loss of hearing will be found very slight. For 
example, there may be no appreciable reduction of hearing power for the 
conversational voice, the initial loss being shown only by a very slight 
reduction of the hearing distance for such sounds as the watch or acoumeter. 
At this stage loss of acuteness for the lower musical tones and increase in 
bone conduction are too slight to be demonstrable. The writer has, 
however, frequently examined patients who could hear tones as low as 18 
d. v. or 20 d. v., yet showed a beginning depreciation of one ear as com¬ 
pared with the other by stating that the sound was distinctly fainter in 
the ear involved. This of course represents the stage of the disease most 
favorable for a practical and permanent cure. As the lesion advances, the 
deafness becomes more noticeable, and the functional reactions assume a 
more characteristic type,— e.g., the lowest musical tones are no longer 
heard and hearing by bone conduction is increased. The high musical 
tones, on the other hand, are heard with undiminished acuteness. In¬ 
crease in bone conduction usually advances with the progress of the lesion. 
I believe, however, that Bezold was justified in his conclusion that the ratio 
between air conduction and bone conduction is never absolutely reversed 
until some structural change— e.g., inflammatory adhesions, fibrous hyper¬ 
plasia, or the formation of new bone (otosclerosis)—has occurred within 


TINNITUS AURIUM 


225 


the oval window or niche, very markedly interfering with the mobility 
of the stapes. If we accept this view,— i.e., that a negative Rinne means 
stapedial ankylosis, partial or complete—it is clear that this test acquires 
added importance as throwing some light upon the character of the lesion, 
and therefore upon the prognosis. If the disease is unilateral or decidedly 
more advanced in one ear than the other, a vibrating tuning-fork held in 
contact with the mid-line of the skull is usually referred by the patient to 
the more diseased ear (Weber’s test). Occasionally, however, it gives 
anomalous or contradictory results, presumably as a result of differences 
in the thickness, solidity, and conductility of the two sides of the skull. 
It is, therefore, of value chiefly when considered in connection with results 
of other tests. What is of greater concern to the patient is the progressive 
loss of auditory acuteness for all sounds by air conduction. Usually his 
first intimation of impaired hearing for the conversational voice comes 
when he first experiences auditory strain at the theatre or in church, or 
at about this time he may notice that he occasionally loses the drift of 
a general conversation,— e.g., at a dinner party. Yet in talking with 
one or two persons he experiences absolutely no difficulty. From this 
stage, years may elapse before the deafness reaches the point where even 
with one or two persons conversation becomes difficult. It is, unfor¬ 
tunately, at this advanced stage that many patients first apply to the 
aurist for help. 

As in tubal catarrh, but to a smaller degree, the deafness in these cases 
varies from time to time,— e.g., with the season of the year, with weather 
changes, and to some extent with changes of climate. As the lesion ad¬ 
vances and the deafness becomes more pronounced, these periods of tem¬ 
porary improvement become less frequent and noticeable. 

Tinnitus Aurium. —Patients- suffering from chronic catarrhal otitis 
media differ very greatly in their subjection to this troublesome symptom. 
To some extent it is present in nearly every case. In some cases, however, 
the subjective noises are so slight as not seriously to disturb the patient, 
and sometimes he is obliged to concentrate his mind upon them before he 
can affirm that they are present. In other cases the loud head noises are 
the patient’s chief concern, and, if he be a nervous individual, they may 
become a veritable scourge. In nearly all cases the subjective noises vary 
greatly at different times, or at least the patient is more troubled by them 
at certain times than at others. The character of the sounds varies greatly, 
as described by different individuals: Usually they are high-pitched. 
Sometimes the patient describes two distinct sounds which are heard 
synchronously in the same ear. While treatment which is successful in 
improving the hearing frequently relieves also the subjective noises, this 
is not by any means invariable. It is best, therefore, to discourage the 
patient from concentrating his attention too closely on this illusive symp¬ 
tom, which may be among the last to be relieved. 

Pain .—While it is true that earache is not a characteristic symptom 
of chronic middle-ear catarrh, I do not believe that ear pain should be 
15 


226 


NON-SUPPURATIVE DISEASES OF MIDDLE EAR 


entirely omitted from the symptomatology of the disease. The writer, 
who has himself suffered from chronic catarrhal otitis media, has occasion¬ 
ally experienced pain in the ear,—sometimes starting quite sharply, but 
usually soon assuming the character of a dull, trying, but not unbearable 
earache, lasting a few hours or sometimes a day or two. I know that many 
sufferers have these periodic ear pains in chronic catarrhal otitis media. 
Many do not. In those cases in which they occur, I believe that they are 
in some way related to periods of active progress or exacerbation of the 
lesion. 

Vertigo. — A comparatively rare phenomenon in chronic catarrhal 
otitis media is subjective vertigo. Usually it amounts to little more than 
slight dizziness lasting but a few moments. Apparently it is not rotary 
in character,— i.e., it is not attended by the impression of the rotation of 
surrounding objects,—but is rather a momentary “ light-headedness ,” 
induced by suddenly rising from a stooping or the recumbent position, 
e.g.y after stooping to tie the shoes, on getting out of bed in the morning, 
etc. The exact causation is not known, the theory usually advanced, that 
it is caused by disturbance of intra-labyrinthine pressure brought about by 
inward displacement of the ossicles, being merely a hypothesis, and far 
from convincing. 

Physical Signs. —Inspection by reflected light reveals almost invari¬ 
ably a retracted drum membrane, the short process appearing more than 
usually prominent, and the hammer handle being displaced inward and 
backward. In some cases the hammer handle is so far rotated inward as 
to appear much foreshortened, or to occupy nearly a horizontal position. 
In others, in which inward rotation is less marked, the hammer handle 
appears much broader than in the normal ear, this being due possibly to 
slight rotation upon the long axis, or to the folding about it of a thickened 
and relaxed membrana tensa. The light reflex is almost invariably changed, 
—being either absent, or reduced to a mere line or point, or broken up 
into two or more points of light. The commonest type of divided reflex is 
seen at a point of light in front of and below the umbo, and a second 
crescentic or curvilinear reflex lying parallel with the peripheral edge of 
the membrana tensa in the antero-inferior quadrant. When retraction is 
marked, the posterior fold and the annulus tendinosus appear unusually 
prominent. The physical signs of retraction are practically the same as 
are seen in acute tubal catarrh (Figs. 94, 95, and 96). 

In some cases the earliest stages of the disease are attended by an 
effusion of serum into the tympanic cavity. This fluid rarely or never 
fills the cavity, but may rise well above the level of the floor of the bony 
canal. A condition described in many text-books, but rarely seen, is 
that of a hair-like line running more or less horizontally across the 
membrana tensa, representing the upper surface level of this fluid. 
Naturally such a line would change its direction with changes in the 
position of the head. 

Other than the physical signs of retraction, the drum membrane may 



PHYSICAL SIGNS 


227 

present no visible evidences of disease. On the other hand, there may be 
certain abnormalities due to structural changes. 

Calcareous Thickening .—The drum membrane may present the ap¬ 
pearance of being thickened within certain well-defined areas as if by a 
chalky deposit upon its inner surface or within 
its structure. These localized deposits are often 
crescentic in shape and confined to the posterior 
segment (Fig. 138), but may take any form and 
occupy any part of the membrana tensa. They 
are commonly regarded as calcareous deposits 
resulting from a rheumatic diathesis. Appar¬ 
ently they do not per se cause much disturbance 
of function, since they are frequently seen in 
persons of normal hearing. 

Tubal Conditions .—During catheter inflation the 
sounds through the diagnostic tube may be faint, 
indistinct, and distant,—indicating an obstructed tube through which 
little or no air enters the tympanic cavity. This, after several compres¬ 
sions of the bulb, may be succeeded by a blowing sound, giving the 
impression of sound originating in or near our own ear, indicating that 
the tube has suddenly opened under the pressure of air from the inflating; 
apparatus. This sudden and very marked improvement in the character 
of the sound while inflation is in progress usually means that congestion 
plays a prominent part in the tubal lesion. 

In other cases air may be heard entering the tjunpanum from the 
start, the sounds being unmistakably tympanic in character, but accom¬ 
panied by moist rales. Such sounds usually indicate an exudative inflam¬ 
mation of the tube, accompanied by an increased secretion of mucus, 
which partly occludes its lumen. Not infrequently such rales disappear or 
become fainter and less frequent during inflation, as a result of displacement 
of the tubal secretion which is expelled into the pharynx by the return air 
current. 

Structural narrowing of the tube is characterized by a sound of tym¬ 
panic quality, but fainter and of higher pitch than is normally heard,— 
fainter by reason of the small volume of air entering the tympanum, the 
higher pitch being explained by the reduced calibre of the tube. Absolute 
closure of the tube, which is exceedingly rare, would be indicated by 
complete absence of sound characteristic of air entering the tympanum. 

Obviously no trustworthy deductions can be drawn from catheter 
inflation until the student has acquired sufficient technical skill to feel 
confident of his ability to place the tip of the catheter in its correct posi¬ 
tion in the pharyngeal end of the tube. 

Besides determining the tubal condition, the otoscope also throws 
some light upon the tympanic lesion, particularly as to the presence of 
two conditions occasionally resulting from this lesion,—viz., the pres¬ 
ence of fluid and relaxation of the drum membrane. 



Fig. 138.—Thickening due to 
calcareous deposits. 





228 NON-SUPPURATIVE DISEASES OF MIDDLE EAR 


In some cases of chronic hypertrophic otitis media, a limited amount of 
mucoserous fluid collects in the lower part of the tympanic cavity. Usually 
it is not sufficient in amount to influence the position of the drum mem¬ 
brane, and may be quite indeterminable by inspection. In such a case 
the inflation sound is modified by a series of bubbling rales. The sound is 
so distinctly characteristic of the passage of air through fluid as to be quite 
unmistakable. As a comparatively rare result of inflation in these cases, 
a number of bubbles may be blown up upon the inner surface of the mem- 
brana tensa, which then become visible through the membrane by reflected 
light. 

Relaxation of the drum membrane is demonstrated during inflation 
when each otoscopic sound begins with a distinct snap. Inflation of the 
normal ear does not give rise to a percussion sound due to the impact of 
air upon the drum membrane; it begins and ends as a moderately low 
blowing sound. With moderate relaxation of the drum-head, there is 
heard with each inflation a short snap, immediately followed by the 
characteristic “blow.” With extreme relaxation, there are two distinct 
and characteristic flapping sounds,—one at the beginning of inflation 
as the relaxed membrane is blown outward, and a second at the end, 
due to its recoil. In this way we frequently become aware of marked 
changes in tension which may be absolutely indeterminable by inspec¬ 
tion alone. 

This loss of normal tension, or relaxation, may be further corroborated 
by means of Siegel’s otoscope. 2 Through the speculum of this instru¬ 
ment the relaxed membrane is seen to execute exaggerated movements,— 
inward against the inner tympanic wall and outward into the auditory 
canal,—as the air in the meatus is alternately compressed and rarefied. 
At the same time we may note a characteristic of the relaxed drum 
membrane which accounts in large part for the resulting deafness,— 
viz., the relatively small influence which wide movements of the relaxed 
membrane exert upon the hammer handle, and therefore upon the ossic¬ 
ular chain. 

The hearing in chronic hypertrophic otitis media is in nearly all cases 
improved as an immediate result of a first inflation. In the early stages 
this improvement is especially marked. As the disease advances and the 
pathologic changes within the tympanum involve more seriously the 
ossicular joints, the functional gain following inflation is naturally less 
pronounced. 

Chronic hypertrophic otitis media tends to gradual but progressive 
impairment of hearing. Whether the functional loss finally disables the 
patient for enjoying the society of his fellows depends to some extent 
upon whether he is fortunate enough to come early under proper care, 
and also upon the character of the lesion. It is conceivable that two cases 
developing with the same initial severity may within the same period of 


2 See Fig. 59, page 59. 





TREATMENT 


229 


years reach very different grades of deafness, from the fact that the hyper, 
trophic process may in one case involve chiefly the regions of the ossicular 
joints, and in the other may be spread over regions of less functional im¬ 
portance. Fortunately, the disease may enjoy periods of apparent qui¬ 
escence, and, even when this can not be affirmed, the patient may be well 
past middle age before his deafness becomes a serious handicap in life. 
There is, however, a numerous class of patients with whom impairment of 
hearing begins very early in life and progresses rapidly, so that the indi¬ 
vidual is seriously hampered at a time when his career is still in the forma¬ 
tive stage and his best energies still called for. 

Prognosis. In the very early stages the disease is probably a curable 
one. In its later stages, when the pathologic basis of the symptoms is 
found in gross morbid changes which can no longer be corrected, the 
patient s symptoms may be relieved and his hearing for a time improved, 
but the lesion is no longer curable. 

Treatment. —It is clear that this lesion may give rise to conditions 
differing widely in their mechanical influence upon sound-conduction. 
Thus, in one case deafness may be due very largely to tubal obstruction 
causing retraction of a relatively normal drum membrane, while in another 
the tube may be patent and the deafness due chiefly to abnormal relaxa¬ 
tion of the drum-head. In still a third variety neither tubal obstruction 
nor relaxation of the drum-head may be marked, the deafness depending 
chiefly upon adhesive processes involving the oval window and stapes. 
Obviously successful treatment demands recognition of the mechanical 
cause of deafness. 

Care of the Nose and Nasopharynx .—As a preliminary measure, the nose 
and nasopharynx should be carefully examined and any lesion or condition 
interfering with nasal respiration, or acting as a predisposing cause of 
tubal congestion, should be corrected. Preliminary to the use of the 
catheter, the nose and nasopharynx should be sprayed with some alkaline 
cleansing solution (Dobell’s, alkalol, normal salt solution). This periodic 
flushing of the nasal spaces is in itself distinctly beneficial in some cases. 
When the turbinates and the nasal mucosa are in a state of chronic con¬ 
gestion or turgescence, the occasional application of argyrol is often of 
value. Under its influence, the congestion usually subsides and the mucous 
membrane regains a more normal tone and appearance. Argyrol may be 
applied twice or three times a week,—either locally in 25 per cent, solution 
by means of a cotton applicator, or in 5 per cent, solution in the form of a 
spray. 

The home use by the patient of cleansing sprays followed by oil sprays 
leads to improvement in some cases, in others seeming rather to excite or 
perpetuate a subacute form of nasal congestion or irritation. Their results 
should, therefore, be carefully watched. 

Local Treatment .—The Eustachian tube is probably in most cases 
the starting-point of this lesion and is our logical point of attack. If the 
condition here is chiefly one of venous congestion, it will in most cases 


230 NON-SUPPURATIVE DISEASES OF MIDDLE EAR 


respond to the measures outlined under chronic tubal congestion, which 
need not be repeated in detail here. 

In all cases in which the tubes are partially occluded, the local treat 
ment should begin with inflation, preferably by catheter. Inflation should 
be repeated at regular intervals, at first on alternate days, this being con¬ 
tinued as long as progressive improvement in hearing can be demonstrated. 
By occasional retesting, the results being compared with those of the ori¬ 
ginal functional examination, it will be easy to gauge the results of treat¬ 
ment. When the functional gain reaches a point beyond which no improve¬ 
ment can be demonstrated, the inflations should be stopped, or practised 
only at considerably longer intervals. 

In many cases the disturbance of the tubal function is due largely to per¬ 
sistent inflammatory changes in the pharyngeal end of the tube, in which 
case the local use of astringent drugs forms an essential part of the treat¬ 
ment. They are applied by means of a cotton applicator bent to a curve 
similar to that of the Eustachian catheter, and introduced catheter-fashion 
into the mouth of the tube. In my experience, nitrate of silver in solution of 
gr. x-xxx ad 5 j, and argyrol in 25 per cent, solution, are the drugs which give 
the best average results. While nitrate of silver is usually well tolerated by 
the tubal mucosa, it is best to begin with a weak solution,— e.g., gr. x ad g j, 
—-and later increase the strength to gr. xxx to the ounce, which accomplishes 
all that would result from a stronger solution and is less irritating. This drug 
should not, as a rule, be applied to the tube oftener than once in seven days. 
It causes considerable burning discomfort at the time, which, however, usu¬ 
ally subsides within from thirty minutes to an hour, leaving the tubes 
clearer. Its value may be considered proved in those cases in which the 
beneficial results of inflation are thereby prolonged or rendered more stable. 
There are cases, however, in which nitrate of silver increases tubal conges¬ 
tion and is distinctly harmful. I have personally found argyrol of more uni¬ 
versal value than nitrate of silver. It is quite as astringent as the latter, has 
very decided antiseptic value, and, so far as I have been able to observe, is 
practically non-irritating. It may be used in solutions from 25 to 50 per cent., 
and as often as twice or three times a week. Next to nitrate of silver and 
argyrol, I have found chloride of zinc in 2 to 4 per cent, solutions of most 
value in these cases. 

Should inflation and the local use of astringents fail to restore the func¬ 
tional activity of the canal, the Eustachian bougie must be employed. In 
the author’s opinion, there are but three clearly defined indications for the 
use of the Eustachian bougies: (1) to determine and locate a point of local 
narrowing, or constriction; (2) to overcome a constriction due to inflamma¬ 
tory adhesions within the membrano-cartilaginous portion of the tube; and 
(3) in certain cases of obstinate tubal congestion, in which the passage with¬ 
out force of a small bougie helps to re-establish the tubal function and opens 
the way for the local or direct application of astringent drugs. Other than 
the above definite and distinct indications, I believe that the frequent use of 
bougies is likely to do more harm than good. 

Eustachian bougies are made of whalebone, celluloid, or certain com- 


USE OF EUSTACHIAN BOUGIE: TECHNIC 


231 


positions in which gum elastic is a prominent constituent. They all 
terminate in an olive-shaped enlargement or bulb. This terminal enlarge¬ 
ment is of diagnostic value in determining the exact position of any local¬ 
ized constriction, in that the stricture offers resistance to its passage 
inward, and again to its withdrawal. Thus, a bougie may pass easily 
through the tube until it meets resistance from a localized constriction. 
Passing this, it may enter the tympanum without further opposition or it 
may encounter and pass a second stricture. Owing to its terminal bulb, 
its withdrawal is again opposed at the points of resistance previously 
noted. In this way one or more strictures may be determined. The size 
is measured by the diameter of the terminal bulb, and varies from a half 
millimetre or less to one and a half millimetres, the latter measurement 
being the largest that should be used. Of the different kinds of bougies, 
the celluloid are much more pliable than the whalebone, following the curve 
of the tube better, and being therefore less likely to create a false passage. 
Most of the composition bougies are open to the objection that they soon 
become rough, increasing the danger of injury to the tubal mucosa. 

As to the size of bougie to be used, whoever attempts this rather deli¬ 
cate procedure should remember that the average normal tube at the 



Fig. 139.—Celluloid bougies (calibre and length reduced). 


isthmus is one and a half millimetres in diameter; some are smaller. If 
we employ a bougie which is too large for the tube, we may by the applica¬ 
tion of force carry it beyond the isthmus, but in doing so may crush or cut 
the mucous lining against the beginning of the bony tube, giving rise to an 
annular cicatrix whose subsequent contraction may cause the most in¬ 
tractable kind of stricture. Ordinarily a bougie with a bulb one millimetre 
in diameter should first be tried. If it meets too much resistance at the 
isthmus, it is better that it be withdrawn and a smaller one substituted. 

Technic .—-As a preparatory step, we will assume that the nose and 
nasopharynx have been thoroughly sprayed with Dobell’s or other cleans¬ 
ing solution; that the catheter of malleable silver has been sterilized by 
boiling; that the celluloid bougie, which cannot be boiled, has been cleansed 
in alcohol and dried with sterile gauze. 

We must also assume that the physician has clearly in mind the fol¬ 
lowing facts, without which he cannot work intelligently: 1, that the Eus¬ 
tachian tube in adults varies from 31 millimetres to 38 millimetres in length; 
2, that its narrowest part, the isthmus, is at the junction of the bony with 
the membrano-cartilaginous portion of the tube; and 3, that the end bulb of 
the bougie will reach the isthmus when it has passed beyond the terminal 
opening of the catheter to a distance varying between 20 and 25 millimetres. 

Obviously we must adopt some method by which the physician may 
know at any time just how far the bougie has passed out of the catheter 
and into the Eustachian canal. In practice I meet this necessity in the 























232 NON-SUPPURATIVE DISEASES OF MIDDLE EAK 


following way. Taking, for example, a celluloid bougie, I pass it through 
the catheter end to a length of about 38 millimetres, or about one and a 
half inches (Fig. 140). Practice soon enables one to gauge this measure¬ 
ment quite accurately by eye. I now bend the opposite, or proximal, end 
quite sharply downward over the edge of the large end of the catheter. 
The bougie retains this bend or angle (6). Now, when the catheter is 



in proper position in the patient’s nose and pharynx and I have intro¬ 
duced the bougie, I know, when my guide-bend is 38 millimetres from 
the outer extremity of the catheter, that the tip of the bougie is just enter¬ 
ing the canal. As the bougie is advanced into the canal, I am able at any 
time to compute the distance it has traversed by mentally deducting from 
38 millimetres the distance remaining between the expanded extremity of 
the catheter and the bend in the bougie. 

The bougie should be passed very slowly and with little application of 
force. If one uses a very small bougie, it may traverse the whole length of 
the canal with no appreciable resistance. With a terminal bulb one milli¬ 
metre in diameter, one will almost invariably meet with a sufficient in¬ 
crease in resistance at the isthmus to inform one that the bougie has 
reached this narrowest point of the canal. If the isthmus can not be passed 
without the use of considerable force, it is better to withdraw the bougie 
and either employ a smaller one, or try the same bougie at a later sitting 
after very thoroughly shrinking the canal with cocaine or adrenalin. In 
many cases the passage of a bougie of proper size is followed within a few 
days by a very noticeable improvement in the patency of the tube. 

Yankauer 3 has devised a set of Eustachian applicators, bougies, and 
sounds, and described in detail a systematic method of dilating a constricted 
tube, which, while founded upon methods long in use, represents a useful 
technical advance. By this method it is possible not only to locate, but 
also to determine the extent, measured in millimetres, of the constricted 
portion of the tube. This constricted portion is then anaesthetized and 
exsanguinated by a 5 per cent, solution of cocaine in adrenalin, 1 to 2000, 
carried into the tube by a specially devised cotton applicator. Following 
this, inflation demonstrates whether the constriction is due to congestion 
or to inflammatory infiltration of the tubal mucosa. If due to the former, 


3 Yankauer: The Isthmus of the Eustachian Tube, A Contribution to the 
and Treatment of Middle-ear Disease, Laryngoscope, July, 1910. 


Pathology 















TREATMENT OF EUSTACHIAN STENOSIS 


233 


application of 25 per cent, or 50 per cent, argyrol solution is made to the 
diseased portion. If dependent upon inflammatory infiltration, the appli¬ 
cation of argyrol is preceded by the passage of the Eustachian sound, 
which is allowed to remain in place five or ten minutes. While this method 
represents a useful initial measure in certain cases, its frequent repetition 
as advised by Yankauer, does not impress the writer as advisable, or as 
altogether without risks. 

The handles of Yankauer’s instruments are provided with a graduated 
scale, enabling the physician to tell at any moment the exact distance to 
which the bougie or sound has entered the canal. 

The Electric Bougie {Duel ).—Still another method of dilating an obsti¬ 
nate stricture of the tube is by the so-called “electrolytic method” devised 
by Dr. A. B. Duel, of New York. Basing his experiments upon the hypoth¬ 
esis,—which is an accepted fact in electrotherapeutics,—that contact of 
the negative pole of a galvanic current favors absorption of inflammatory 
products, he subjected a number of patients, with tubal strictures which 
had resisted other methods, to the following treatment: Using a galvanic 
battery provided with a reliable rheostat and milliamperemeter, a bougie 
constructed of gold wire was connected with the negative pole, the positive 
electrode being held in the patient’s hand. This bougie was passed through 
a silver catheter, insulated by a covering of rubber tissue, and slowly 
advanced until its progress was blocked by the stricture. The current was 
then gradually turned on to a strength varying between two and five 
milliamperes. In many cases it was found that at the end of from two to 
five minutes the bougie could be advanced without force. 

A somewhat alarming accident, which has been recorded by several 
aurists, is the breaking or separation of the distal end of the bougie within 
the Eustachian tube. This has never occurred in the writer’s experience, 
and he has found this treatment of decided value in certain cases in which 
all other methods of dilatation had failed. It is an agent which should 
not be used carelessly, and whoever wishes to employ it should follow 
carefully the technic as described by its sponsor. 4 

The patency of the tube having been restored so far as catheter inflation 
may indicate, the patient should for a time be carefully observed for the 
purpose of determining whether the tubal function has also been re-estab¬ 
lished. Every aurist has had experience with cases in which inflation 
results in an apparently normal air current to the tympanum, yet with 
each return of the patient the drum membrane is found retracted. Func¬ 
tional improvement following inflation is, therefore, only temporary. 
This condition would seem fairly positive proof that, while the tube itself 
is patent, its function has not been resumed. Upon such a case a com¬ 
parison of the results of inflation by catheter and by the Politzer method 
may throw considerable light. Supposing, for example, in a case of uni¬ 
lateral disease that catheter inflation reveals a normally patent tube and 

-— —---■ ■ ■— 1 — - ■■■■■— — 1 ■ — ■ ■ - -i 

4 Duel: The Technic of Eustachian Electrolysis, Trans. Am. Lar., RhinoL, and 
Otol. Society, 1909. 




234 NON-SUPPURATIVE DISEASES OF MIDDLE EAR 


yet by the Politzer method little or no air reaches the tympanum, the 
evidence of obstruction at the pharyngeal mouth of the tube would seem 
to be clear. The mechanical cause of this obstruction may or may not be 
visible by means of the postnasal mirror, being due possibly to one or other 
of the following causes,—viz.: (a) remnants of adenoid tissue remaining 
in the fossa of Rosenmiiller, occasional congestion of which closes the tube 
by pressure; (b) chronic oedema or swelling of the lips of the pharyngeal 
mouth of the tube, giving them a valvular action under pressure; (c) un¬ 
relieved oedema within the mouth of the tube, beyond which the catheter 
passes; and, lastly, (d) there may possibly be cases in which, as a result of 
hyperplastic thickening or induration of the nasopharyngeal and tubal 
tissues, the pharyngeal muscles no longer act effectively upon the pharyn¬ 
geal end of the tube. These conditions suggest their appropriate treatment. 

When finally the function of the Eustachian canal has been re-estab¬ 
lished, the further treatment will naturally depend upon the interpretation 
of the tympanic condition. If the subjective symptoms have been relieved 
and a reasonable improvement of hearing obtained, it may be better to 
suspend all treatment, instructing the patient to return within three to 
six months in order that the permanency of the results may be tested. 
On the other hand, if symptoms are present depending apparently upon 
tympanic hypertrophy or congestion, a persistent effort should be made to 
correct these conditions. 

Since any further treatment which may be required in these cases 
conforms in a general way to that indicated in the hyperplastic form of 
chronic otitis media, the subject may with advantage be deferred to be 
considered jointly with the treatment of that disease. 

Chronic hyperplastic otitis media (sometimes called dry catarrh 
of the middle ear) is characterized by an excessive production of new 
connective tissue within the tympanic mucosa. In the drum membrane 
this hyperplasia may involve not only the mucous membrane, but also 
the fibrous layers of the membrana tensa, which may to a greater or less 
degree be replaced by new connective tissue. The mechanical results of 
these changes vary logically with the regions and tympanic structures in¬ 
volved. Wherever the joint structures of the ossicular chain are involved, 
the contiaction of new connective tissue may react unfavorably upon ossi- 
culai mobility. \V ith the membrana tensa, on the other hand,while con¬ 
nective tissue hyperplasia may lead to apparent thickening, the loss or 
atrophy of the normal fibrous layers may, and usually does, result in a loss 
of normal tonicity, 01 lelaxation, which constitutes one of the chief factors 
in the mechanics of obstructive deafness. 

All authors agree that the condition above described is often a late stage 
of the hypei ti ophic foim of chronic middle-ear catarrh, beginning with 
well-marked round-celled infiltration, and ending in the conversion of the 
newly foimed lound cells into fibrous connective tissue. The same process, 
taking place within the Eustachian tube, may give rise to widely different 
end-results, e.g., (a) the deposition of new tissue may be so extensive as 


CHRONIC HYPERPLASTIC OTITIS MEDIA 


235 


nearly to occlude the isthmus of the tube, resulting in an organized obstruc¬ 
tion or stenosis very difficult to correct; or (b) the hyperplastic process 
being less marked, contraction of a moderate amount of new connective 
tissue gives rise to an abnormally wide and open tube. 

The lesion may be further complicated by the presence of fibrous 
bands passing between the ossicles and adjacent tympanic surfaces. They 
may, for example, bind the head or crura of the stapes to the walls of the 
oval niche, adding greatly to the impairment of hearing. Such adhesive 
structures probably always represent an earlier hypertrophic or exudative 
stage in which swelling or oedema was a more or less prominent feature. 

Symptoms. — Since they in many respects resemble those already 
described under chronic hypertrophic otitis media, the symptoms may be 
dealt with briefly. 

Usually when the diagnosis is made the hearing is already considerably 
impaired, there being noticeable loss of hearing for the lowest musical 
tones, and hearing by bone conduction being appreciably prolonged. The 
ratio between hearing by air conduction and bone conduction may or 
may not be reversed, actual reversal not taking place until the deafness 
is very pronounced. As compared with chronic hypertrophic otitis 
media, it has seemed to me that sufferers from this lesion show often a 
loss of hearing for the conversational voice and whisper out of proportion 
to the demonstrable changes in tone limits and bone conduction. For 
example, the patient may have difficulty in hearing a moderately loud 
whisper at 5 or 6 feet, and yet may hear forks as low as 36 or 40 double 
vibrations per second, and bone conduction may be only moderately 
increased. The degree of deafness is also less variable, neither weather 
conditions nor changes of season or climate influencing it so markedly as 
in the hypertrophic form of middle-ear catarrh. 

Paracusis (Willis ).—A condition which sometimes accompanies the 
deafness of this lesion is known as paracusis Willisii. It is present when an 
individual with advanced deafness can understand conversational speech 
better in the presence of loud surrounding noises than in a quiet room. 
Thus, some patients, who are ordinarily extremely deaf, hear with com¬ 
parative ease while traveling in a railway-car or when walking in a noisy 
street. There are two theories in accordance with which this phenomenon 
is explained,—viz.: (1) The tympanic theory,— i.e., that, with pronounced 
tympanic changes, the ossicular chain loses the power of responding ade- - 
quately to the conversational voice; but that, when set in motion by such 
gross sounds as the noises of the street or of a railway-car in motion, they 
regain for the time their responsiveness to the more delicate sound waves 
involved in conversational speech. (2) The labyrinthine theory is that in 
cases of very advanced deafness, even though the lesion may be of 
tympanic origin, the auditory nerve becomes more or less torpid and irre¬ 
sponsive to the voice sounds, but that when stimulated by loud noises it 
becomes simultaneously more responsive to the more delicate and complex 
sound waves of the conversational voice. 


236 NON-SUPPURATIVE DISEASES OF MIDDLE EAP 


Paracusis is seldom present in chronic hyperplastic otitis media 
except in the advanced stages in which the ratio between air con¬ 
duction and bone conduction is reversed (negative Rinne). It is 
also very commonly present in advanced stages of otosclerosis. It 
is probably, therefore, in some way related to conditions bringing 
about fixation of the stapes, and to this extent is of some importance 
as bearing upon the prognosis. 

Tinnitus aurium, though usually present, varies greatly in different 
cases, either in its intensity or in its impression upon the patient. Some 
patients, while stating that the subjective noises are continually present, 
do not seem to be greatly disturbed thereby. Others, either by reason of 
their loud character or through anxiety as to their significance, are made 
exceedingly nervous or unhappy by them. A not uncommon impression 
among those who suffer from tinnitus is that their difficulty in hearing is 
due chiefly to the confusion incident to the subjective noises, rather than 
to actual impairment. “I could hear perfectly if it were not for these 
head noises,” is a statement with which every aurist is familiar. Fortu¬ 
nately, many people with incurable ear lesions become so accustomed to 
continual head noises as actually to be unconscious of them during the 
day, when the noises of the street and the interests of the hour serve to 
distract their attention. Undoubtedly individuals of trained will power 
are less disturbed than the weak, nervous, or neurasthenic. 

As with chronic hypertrophic otitis media, vertigo is a comparatively 
rare phenomenon, and when it does occur is usually little more than a 
momentary dizziness, sometimes, however, recurring with annoying per¬ 
sistence. When severe attacks of vertigo, accompanied by disturbance 
of static equilibrium, occur in this lesion, careful functional examination 
will usually establish other clearly defined evidences of labyrinthine 
involvement. 

Physical Appearances of the Drum Membrane.— While the Eus¬ 
tachian canal may be not only patent but abnormally wide, it is a curious 
fact that the drum membrane is in most cases distinctly retracted. The 
frequent coincidence of a widely open tube and a retracted membrane may 
in some cases be accounted for as being the result of adhesions between the 
hammer handle and promontory, shortening of the tensor tympani, etc. 
Probably much oftener it is the result of an earlier hypertrophic stage 
during which tubal obstruction led to prolonged retraction of the mem¬ 
brane, the resulting loss of resiliency preventing its subsequent return to 
the normal position. 

The most characteristic appearance, however, is that of moderate 
thickening, the membrana tensa appearing to be not only thicker but 
to have lost in some degree its characteristic sheen or lustre. This con¬ 
dition is usually the result of an increase of connective tissue at the ex¬ 
pense of the normal fibrous layers of the membrana tensa. The apparent 
thickening is often most marked at the periphery and in the central area 
immediately surrounding the umbo. In some cases the deposition of new 
connective tissue may be plainly seen in the form of opaque lines running 


PHYSICAL SIGNS 


237 


in various directions through the tense membrane, most often radiating 
from the umbo or hammer handle to the periphery. Such a drum mem¬ 
brane, if examined with Siegel’s otoscope, will not infrequently be found 
to be abnormally relaxed, both anterior and posterior segments making 
exaggerated movements as the air in the auditory canal is alternately 
compressed and rarefied. 

Atrophy of the Drum Membrane .—The drum membrane may present 
exactly the opposite appearance to that just described, the whole mem- 
brana tensa being abnormally thin and transparent. This change is 
probably the result of atrophy and partial disappearance of its fibrous 
layers under the pressure of a moderate deposition of new connective 
tissue. The membrane in consequence is exceedingly thin, transparent, 
and so relaxed as to exhibit in some cases exaggerated degrees of retraction. 
Tympanic structures not clearly visible through the normal membrane 
come therefore plainly into view through the depressed and attenuated 
membrane. Thus, the incudostapedial joint and niche of the round win¬ 
dow may be quite prominent, the membrane being applied so closely to 
the inner tympanic wall as almost to give the impression that one is look¬ 
ing directly at the tympanic structures. This is the type of membrane 
which may be easily ruptured by catheter inflation even with model ate 
pressure. Naturally the physical picture is greatly altered by inflation 
but the lack of normal tension favors quick return to the condition ot 

exaggerated retraction. , 

There are also cases in which the membrana tensa undergoes atrophy 

only in certain regions, the rest of the membrane being apparently normal. 
This condition is in some cases easily recognized by the greater trans¬ 
parency of the area involved; in others, there may be no structural change 
which the eye can appreciate, the condition being detected only w 1 e 
examining the drum membrane with a Siegel otoscope, when the atrophied 
part is seen to balloon out into the meatus independently of the surround¬ 
The immediate effect of inflation upon the hearing depends upon a 
variety of conditions,— e.g., patency or structural narrowing of the tube; 
the degree of relaxation of the membrana tensa; and, more than any other 
condition, upon the presence of adhesive processes involving the stapes and 
margins of the oval niche. Whatever the condition may be, the immedi¬ 
ate effect of a first inflation is usually in the direction of an improvement 
in hearing. As a rule, however, the functional gain is not so pronounced as 
that which is obtained in chronic hypertrophic otitis media. This is to 
some extent a differential point between the two conditions When the 
tube is greatly narrowed at the isthmus, the otoscopic sound during infla¬ 
tion is of reduced volume and higher pitch than is normally heard. )n 
the other hand, with an abnormally wide tube, one hears a very low full, 
and often rough, blowing sound. A very common accompaniment of the 
pathologically wide tube is marked relaxation of the drum membrane. 
During Inflation one may hear, therefore, not only the low, rough, blowing 


238 NON-SUPPURATIVE DISEASES OF MIDDLE EAR 


sound of the wide and probably dry canal, but in addition the character¬ 
istic flapping sound of the relaxed membrane. In such a case the increased 
calibre of the tube and loss of tension in the membrana tensa are each in 
their way expressions of the same morbid process,—viz., atrophy and 
partial disappearance of normal tissue elements. 

The use of Siegel’s otoscope is an important part of the examination of 
these cases, enabling the physician to detect adhesions between the hammer 
handle and promontory, or between the drum membrane and intratympanic 
structures. During rarefaction of air in the meatus, the free portions of 
the drum membrane are sucked outward into the canal, leaving the points 
of adhesion depressed and in conspicuous view. The Siegel otoscope also 
enables one to determine loss of tension— i.e., relaxation—of the membrane, 
either localized or involving the whole membrana tensa. 

Course of the Disease; Prognosis. —The tendency of the disease 
is toward slowly increasing deafness. The possibilities of treatment 
' depend in each case upon the stage of the disease, the degree of deafness, 
and the physician’s ability to interpret correctly the mechanical cause of 
the deafness. In some cases local treatment fails utterly to influence the 
symptoms. In most cases, however, something may be accomplished 
either in the way of improving the patient’s hearing or conserving that 
which remains to him. 

Treatment. —Since the treatment of chronic hypertrophic otitis 
media has been described somewhat in detail, it will suffice here to 

speak briefly of the chief indications in this form of chronic middle-ear 
disease. 

As with all forms of tympanic disease, the Eustachian canal should 
receive first attention. If the tube is found to be structurally narrowed, 
an effort should be made to re-establish its normal patency. For this 
purpose some form of mechanical dilatation is essential. Preparatory to 
the introduction of a bougie, the nose should be thoroughly sprayed 
with some cleansing solution (Dobell’s, Seiler’s, alkalol), and a 4 per cent, 
solution of cocaine should be applied to the pharyngeal end of the tube. 
Using the ordinary celluloid or whalebone bougie, it is best to employ 
first one of the smaller sizes, gradually advancing to the largest size 
which will pass the isthmus without much force. 

A weak point in this type of dilator is in the form of the bougie,— i.e., a 
terminal enlargement or bulb attached to a narrow shaft,—limiting the 
dilation to the passage back and forth of the bulb. To meet this difficulty 
Yankauer has devised a Eustachian sound, the tubal part of which is of 
uniform calibre, enabling one to maintain uniform dilatation throughout 
the constricted portion of the tube. This in some cases gives better re¬ 
sults than the ordinary bougie. 

Whatever instrument is used, its calibre should not be larger than can 
lie made to pass the isthmus with comparative ease,— i.e., without risk of 
injury to the tympanic mucosa. The effort by suddenly applied force 
to pass a large bougie beyond the isthmus may give rise to traumatism 


TREATMENT 


239 


and subsequent cicatrization, leading ultimately to an annular constric¬ 
tion, or stricture, far more difficult of correction than that which we set 
out to relieve. 

Following the sound or bougie, the application of a 25 per cent, solu¬ 
tion of argyrol throughout the entire length of the canal by means of 
a Eustachian applicator may add to the efficiency of this treatment. 

The use of bougies has been advocated by various authorities and for 
various purposes. It has been used, for example, as a means of massaging 
the tubal mucosa, for which purpose a bougie as large as will pass the 
isthmus without force is introduced, and allowed to remain in the tube five 
minutes or more. Professor Urbantschitsch advised that its stimulating 
action be increased by friction,, the bougie being moved rapidly back and 
forth in the dilated tube, a measure which would seem to the author to be 



Fiq. 141.—Eustachian applicator made of No. 5 piano wire 


contraindicated by the inherent risks. With the same end in view, the 
tubal end of the bougie may be dipped into a solution of arygrol or ichthyol 
or into a weak solution of nitrate of silver, and passed thus into the canal. 
Albert A. Gray, of Glasgow, advises that the end of the bougie be smeared 
with an ointment having a one-half per cent, nitrate of silver content, the 
vehicle being lanolin. The bougie thus medicated he allows to remain in 
the tube twenty minutes or longer. All of these measures have in view 
the purpose of increasing the local blood supply of a wide-open and 
sclerotic canal. 

Probably the most effective mode of stimulating the tubal membrane, 
and certainly the best way of applying drugs locally to the canal, is by 
means of a suitable Eustachian applicator. A perfectly practical applicator 
and one which can be easily prepared by the physician, is that long since de¬ 
scribed by Dr. Dench, li consists simply of a piece of No. 5 piano wire cut 
to the proper length, the end of which to a length of about one millimetre is 
sharply bent backward so as to lie in contact with the main wire (Fig. 141). 


240 NONSUPPURATIVE DISEASES OF MIDDLE EAR 


A very small pledget of sterile cotton wound about this is firmly engaged by 
the terminal hook, and cannot be dislodged in the tube. Yankauer’s appli¬ 
cator has the advantage of a convenient handle and greater flexibility (Fig. 
142). With either of these instruments drugs may be applied throughout 
the entire length of a patent tube. In the author’s experience, argyrol in 25 



Fio. 142.—Yankauer’s Eustachian applicator. 


to 50 per cent, solution is the drug giving best results in these cases; it is 
both astringent and stimulating, possesses considerable antiseptic value, 
and is practically non-irritating. It may be applied as often as twice or 
three times a week. 

After all that seems possible in re-establishing normal conditions within 
the Eustachian canal has been accomplished, there is still the question of 
the tympanic cavity proper, and what may be done to restore its lining 
membrane to a condition more nearly approaching the normal standard. 

Upon purely theoretic grounds it would seem that drugs which have 
proved their value as applied to the tube should have a similar field of 
usefulness as applied to the tympanic cavity. That they are not equally 
available is due not to any difference in their local action in the two situa¬ 
tions, but to the comparative difficulty in applying them to the tympanic 
walls. While the introduction into the tympanum of various drugs in 
solution has been mentioned by many distinguished aurists, I have always 
felt that this might be attended with certain risks. My own experience 
has, therefore, been confined largely to the use of one drug, argyrol, ap¬ 
plying it in the following way, viz., the Eustachian canal having been 
cocainized, a few drops of a 25 per cent, solution of argyrol are 
taken up in the end of a catheter, which is then introduced and inflation 
performed in the usual way. In this way a drop or two of the solution 
reaches the tympanum, probably in the form of a spray. If the drum 
membrane is inspected a minute or two thereafter, it will be found to be 
markedly congested. 4 he patient usually experiences a burning sensation, 
but i arely pain. Both the sensation of heat and the redness are temporary, 
and the congestion will usually have disappeared when the patient is again 

seen by the physician. Certain cases have been benefited by argyrol 
used in this way. 

Catheter Inflation. According to my experience the value of catheter 
inflation in the treatment of deafness is distinctly limited. The prolonged 
routine use of catheter, repeated at short intervals, has practically no value 
in correcting ossicular rigidity, and is likely to produce structural changes 
in drum membrane leading ultimately to definite diminution of hearing 








AUDITORY MASSAGE 


241 


While in a general way it may be stated that most cases of chronic 
hyperplastic otitis media are benefited by occasional catheter inflation, 
this statement calls for an accompanying word of caution. Inflation, 
like every other therapeutic measure, has its indications and its contra¬ 
indications, and there can be no doubt that many cases of “chronic deaf¬ 
ness” have been made permanently worse by irrational, routine use of 
the catheter. For example, let us consider a case of extreme atrophy of 
the drum membrane in which the membrana tensa is attenuated, trans¬ 
parent, and appears as if plastered against the promontory. Such a drum 
membrane may be easily ruptured by catheter inflation, and, if this acci¬ 
dent does not occur, the already pathologically relaxed membrane may be 
still further stretched. I have seen cases presenting this extreme degree 
of attenuation and retraction in which a very fair amount of hearing power 
was retained, the drum membrane of course having ceased to fulfil any 
other purpose than that of a protective covering, and the sound waves 
being taken up directly by the ossicles beneath,—possibly being trans¬ 
mitted directly to the incudostapedial articulation. Under these condi¬ 
tions, it may be well at very considerable intervals—certainly not oftener 
than once or twice a month—to practise very gentle inflation simply to 
lift the membrane away from its contact with tympanic structures and 
thus prevent adhesions which, becoming organized, might add seriously 
and permanently to the impairment of hearing. 

Another condition more easily overlooked is that in which the drum 
membrane, though thickened by connective-tissue hyperplasia, has suf¬ 
fered a coincident loss of tension,— i.e., is relaxed. In this condition it is 
clear that catheter inflation is an exceedingly dangerous procedure, since 
its mechanical results are more in the direction of a further reduction of 
tension than of effectively exercising the ossicular chain. 

If, as sometimes occurs, some degree of relaxation of the drum-head 
coexists with tubal or other conditions calling for catheter inflation, it 
may be well to apply a coating of collodion to the membrana tensa. This 
in contracting tends to draw the drum membrane outward into its normal 
position, and to protect it from further stretching under gentle inflation. 

Auditory Massage .—A somewhat perplexing problem in the treatment 
of these cases is the necessity of combating tympanic and ossicular rigidity 
by some form of passive exercise. The method which has been most 
extensively employed for this purpose is what is known as pneumatic 
massage. 

Pneumatic massage is a term applied to passive movements of the 
drum membrane by means of any instrument producing alternate conden¬ 
sation and rarefaction of the air in the external auditory meatus. A very 
large number of such instruments have at various times been placed on 
the market. They are all somewhat similar in design, in that they combine 
the principle of a Siegel otoscope with that of an electric or other motor by 
which the piston is moved rapidly back and forth. 

Such instruments seem to be based upon the theory that whatever 


16 


242 NON-SUPPURATIVE DISEASES OF MIDDLE EAR 


will move the drum membrane and ossicles will improve the hearing. 
They quite ignore the ease with which the adjustment of so finely balanced 
a mechanism may be disturbed. Let us recall for a moment the character 
of this mechanism,— i.e., a system of delicate and sensitively mobile levers 
capable of responding to the slightest movements of the drum membrane, 
and designed to respond to such movements, and to no others, through 
life. Obviously the perfect execution of this function must call for a defi¬ 
nite and proportionate degree of tension in both drum membrane and 
ossicular chain, that of the latter being maintained by the tympanic 
muscles. Clearly the movements of a relaxed membrane can be but im¬ 
perfectly transmitted to a system of heavier bone levers. If, therefore, 
we close the meatus and subject the drum-head to a series of crude exer¬ 
cises in which the ossicles can not possibly take part, it is obvious that the 
net result will be undue relaxation of the membrana tensa and further 
impairment of hearing. 

In any system of tympanic massage we should bear in mind the very 
limited maximum excursions which, according to the investigations of 
Helmholtz, Politzer, and others, the individual ossicles can make in re¬ 
sponse even to experimental movements of the drum-head,— i.e., hammer 
handle, three-fourths of a millimetre, stapes one-fourteenth of a millimetre. 

In some cases a very noticeable gain in hearing has resulted from a 
first treatment by this method. This initial gain has rarely proved perma¬ 
nent, and progressive improvement has never to my knowledge resulted 
from repeated use of this measure. 

The unsatisfactory results of this form of massage are probably ex¬ 
plained by two facts: (1) The movements of the membrana tympani are 
not those which nature requires of it or which are necessary to the trans¬ 
mission of sound waves, and do not therefore exercise the drum membrane 
and ossicles in their normal function. (2) The undue strain to which the 
drum membrane is subjected tends to produce alterations in tension, 
reducing still further the patient’s hearing power. 

It may seem from the above that my purpose is to discourage all efforts 
to exercise the drum membrane and ossicles through the external auditory 
meatus. This, however, is not my intention, since I believe this to be one 
of the most important problems before otologists to-day. 

Preobraschensky, of Moscow, who has made systematic investigations 
of the various methods in use, records his belief that vibratory massage 
with any instrument which fits into and tightly closes the meatus, produces 
such rough and exaggerated movements as to constitute an insult to the 
delicate mechanism involved. With this view I have long been in accord. 5 

Undoubtedly there are many cases which call for some form of ossicular 
massage beyond that which catheter inflation affords. In trying to meet 
this indication, we should bear in mind the following points: The ear- 


5 Kerrison: Notes on Some Very Simple Experiments as to the Influence of Sound 
Waves on Ossicular Rigidity, Jour. Amer. Med. Assoc., December 1 , 1906. 




RATIONAL USE OF TRIED REMEDIES 


243 


piece of the instrument should not be introduced into the meatus so as to 
close the canal. Either it should be held slightly separated from the ear, 
or the ear-piece should be perforated. Tight closure of the canal produces 
exaggerated movements of the drum-head which are distinctly injurious. 
Since the loss of mobility is usually greatest in response to the relatively 
slow vibrations concerned in the production of low musical tones, it would 
seem more rational to employ a rather low vibration rate, using vibrations 
of considerable force or amplitude, rather than very rapid vibrations to 
which the ear still responds with apparently normal ease. For the same 
reason, low musical tones may of themselves be of value in exercising the 
ossicles in cases of beginning tympanic deafness. 

From the foregoing pages it will be seen that the writer has made no 
attempt to describe an inelastic course of treatment which would fit all, 
or even a majority, of these cases. He has tried rather to describe certain 
morbid conditions which may be met with in either the hypertrophic or 
hyperplastic form of chronic otitis media, and to suggest the more rational 
means for correcting the same. 

I believe that we should not make use of too many therapeutic agents 
simultaneously, since by so doing we shall inevitably mask the results of 
the different agents employed. For example, in a foreign clinic the writer 
once saw a considerable number of patients under treatment by a galvanic 
current of moderate strength applied alternately in front of and behind 
the ear for a period of five or ten minutes. To determine the value of 
such treatment, other measures should for the time being be excluded. If 
at one sitting we inflate the tympanum, pass a bougie for purposes of tubal 
dilatation or massage, and supplement these measures by some form of 
external vibratory massage, we shall certainly be at a loss in analyzing 
our results,—whether of functional gain or loss. I believe, therefore, that 
if we are endeavoring to restore the normal calibre of a restricted tube, it 
is best to postpone other local treatment until we are satisfied with the 
mechanical widening of the tube, and are able to determine what functional 
gain, if any, has resulted from this change. Following this plan, and weigh¬ 
ing results by frequent hearing tests, we shall soon know definitely (1) 
whether the patient is being benefited, and (2) to what particular agent a 
demonstrable improvement is due. 

Before leaving this subject, a word must be said as to the constitutional 
or general management of these cases. Undoubtedly some cases of chronic 
middle-ear catarrh have a constitutional basis in subacute or chronic 
gout or rheumatism. When such a diathesis can be determined, the care¬ 
ful physician will recognize its possible bearing upon the tympanic lesion 
and the importance of constitutional remedies. 

In a majority of cases it is difficult or impossible to trace any relation 
between the aural disease and any constitutional disorder. The general 
treatment often narrows itself, therefore, to a regulation of the patient’s 
mode of life,—this including such minutiae as clothing, diet, use of tobacco 
or alcholic drinks, habits of open-air exercise on the one hand or of over- 


244 


OTOSCLEROSIS 


work and excessive confinement to office or business on the other. These 
influences vary so greatly in different cases that they can not be disposed 
of dogmatically. In the case of tobacco, for example, we know that many 
excessive smokers go through life without discoverable ear lesion or dis¬ 
order. When, therefore, a patient with chronic aural disease acknowledges 
to a moderate use of tobacco, I believe that we should investigate rather 
carefully its possible influences before depriving him of a comfort for which 
a more harmful substitute may be found. If we believe that even moderate 
smoking is in a given case harmful to the individual, it should undoubtedly 
be advised against. Excessive smoking is always harmful to these patients, 
either in its effect upon the tubal mucosa or in the influence of the tobacco 
upon the auditory nerve. 

Since all these matters must be discussed more at length in connection 
with otosclerosis, the student is urged to a careful consideration of the 
treatment of that disease. 

OTOSCLEROSIS. 

While no pathological relationship between otosclerosis and disease of 
the middle ear has been demonstrated, the clinical resemblance is in many 
cases so great as to render a differential diagnosis no easy matter. It 
seems best, therefore, that it be considered side by side with the other 
lesions commonly leading to impaired hearing or deafness. 

Definition .—The term otosclerosis is employed to describe the con¬ 
dition in which, independently of the health or intercurrent disease of the 
tympanum, the bony capsule surrounding the labyrinth is the seat of 
chronic non-suppurative disease interfering with the function of hearing. 

Etiology. —With reference to the etiology, it is well to acknowledge 
at once that we have as yet no definite knowledge as to the exciting causes 
of this disease. It has occurred with sufficient frequency in syphilitic 
subjects to lend some weight to the conjecture that syphilis in some way 
influences its inception. Habermann 6 is among those who have held that 
syphilis is a direct cause of the disease. Korner, 7 on the other hand, in 
analyzing the grounds for this belief, could find therein no proof that 
otosclerosis is ever of syphilitic origin. Professor Denker, 8 of Halle, 
made a thorough and careful investigation of 27 cases in which the clinical 
histories were recorded during life and in which the tissues were examined 
post mortem under the microscope. As a result of these studies and a 
review of the literature, Denker concludes that there is no proof that 
syphilis is ever a direct cause of otosclerosis. It now seems probable that 
syphilis is a factor in the progress of the lesion rather than in its causation. 
Thus, otosclerosis in an individual suffering from constitutional syphilis 
is said frequently to run a rapid course leading early to marked deafness. 
Naturally gout and rheumatism are present in a certain proportion of 

6 Habermann: Arch. f. Ohrenh., Bd. lx. 

7 Korner: The Heredity of Otosclerosis, Arch, of Otol., Amer. Edition. 

8 Denker: Die Otosklerose, p. 81-84. 





ETIOLOGY; PATHOLOGY 


245 


cases, but if they have any causal relation to the disease, it is probably an 

indirect one exerted through the anaemia and lowered physical state to 
which they give rise. 

While the disease is sometimes seen in patients who also present evi¬ 
dences of tympanic disease, it seems probable that the two lesions are in 
most cases quite unrelated. Certainly many cases of otosclerosis have 
been observed m which there was complete absence of all signs of tympanic 
disease, past or present. As to whether tympanic disease is ever the 
direct cause of the lesion under discussion, there is still some difference 
of opinion with the consensus of opinion steadily turning to the belief 
that otosclerosis is a pathological entity never secondary to a tympanic 
lesion. This question will be referred to later. 


An etiological factor which heretofore has received scant attention, but 
which is destined to have greater consideration in future, is the influence of 
poisons conveyed through the blood stream from extraneous foci of infec¬ 
tion. If infected tonsils, carious teeth, or pus foci in any part of the body 
may cause inflammatory changes in the articular structures of the larger 
joints, why not also in the joint structures of the ossicular chain? And why 
may not the same metastatic poisons influence—at least in some cases—the 
initial changes in the bony labyrinthine capsule leading eventually to the 
characteristic features of otosclerosis? I believe that the tonsils are des¬ 
tined in futuie to come more frequently, and I hope earlier, under suspicion 
in their possible relation to otosclerosis. 


While it is conceded to be a disease of middle life, usually commencing 
after the twentieth year, Korner has shown that it may occur much earlier, 
recording two cases from his own practice in which the disease was present 
at ten years and fifteen years respectively. Sex seems to influence predis¬ 
position to the extent that women are more frequentlv sufferers than 
men,) e.g., 58.2 per cent, in women, 41.8 per cent, in men (Denker). Her¬ 
edity undoubtedly plays an important part in the spread of the disease, 
as has been proved by Hammerschlag, Korner, Gray, and others, who have 
published family trees showing remarkable reproduction of the disease. 

Morbid Changes. Affecting the Mobility of the Stapes—In the minds of 
many, the association of otosclerosis with bony fixation of the stapes is a 
fixed idea; hence the determination in any case of stapedial ankylosis is 
apt to suggest the presence of otosclerosis. It is obvious that such de¬ 
ductions may lead to faulty diagnosis. 

Firm fixation of the stapes in the oval window or niche may be caused 
by many conditions,—as, for example, the fibrous bands sometimes re¬ 
sulting from chronic hypertrophic otitis media, which may give rise to a 
very high degree of stapedio-vestibular ankylosis. Such processes have 
been very clearly demonstrated by Politzer 9 and others. Another form of 
stapedial fixation occasionally results from middle-ear suppuration, in 
which masses of granulation tissue occupying the oval window recess may 
be transformed first into fibrous tissue, and later as a result of inflammatory 

9 Politzer: Diseases of the Ear, p. 278. 





246 


OTOSCLEROSIS 


changes in the surrounding bone may even be converted into bone 
(Pritchard). 10 It is needless to say that such conditions have no relation 
to true otosclerosis. 

Pathology. —Otosclerosis is a lesion originating, so far as we know, 
in the bony capsule surrounding the labyrinth, and varying in its mechani¬ 
cal results according to the region chiefly involved. Occurring in the region 
about the oval window, it may give rise to ossification of the annular liga¬ 
ment, or rather to its absorption and replacement by bone, with resulting 
osseous fixation of the stapes. In other recorded cases, the morbid pro¬ 
cess has involved intra-labyrinthine structures,— e.g., the spiral membrane, 
—and thus caused deafness without producing stapedial fixation. Fur¬ 
thermore, since foci of the disease have been observed in widely separated 
portions of the petrous bone, there can be no doubt that characteristic 
changes may occur in parts of the labyrinthine capsule not closely related 
to structures essential to the cochlear function, in which case the patient 
would still have otosclerosis, though a diagnosis would not be made on 
account of the fortunate absence of symptoms. 

The morbid process seems to lack any of the characteristic features 
of an inflammatory process. It consists essentially of the absorption of 
the old bone in the region involved and its replacement by new spongy 
bone. The new spongy bone is characterized by Havarsian canals of 
abnormal width, and by large medullary spaces containing numerous 
multinuclear cells and large thin-walled blood-vessels. The new bone is 
also characterized by its strong affinity for haematoxylin and carmine dyes. 
It is differentiated by a distinct line of demarcation from the surrounding 
healthy bone. It may retain its spongy character, or may in time be con¬ 
verted into dense bone. These changes may occur in any part of the bony 
capsule of the labyrinth. The commonest point of attack is that portion 
of the labyiinthine capsule just above and in front of the oval window. 
Occuning in this region, the upper and anterior margins of the window 
undergo the characteristic changes. Absorption of any portion of the 
margin of the oval window cuts off the nutrient supply of the contiguous 
portion of the annular ligament of the stapes (Gray). The ligament 
therefore, is also absoibed, its place being occupied by new spongv bone 
which later may be converted into compact bone. 

The foregoing paragraph appeared in the first edition of this book and 
is as pertinent today as when it was written. In his more recent work on 
otosclerosis. Gray discusses the origin and pathology of the disease more 
from the biologic viewpoint. Drawing upon the storehouse of his exten¬ 
sive knowledge of comparative anatomy, he pictures for us the gradual 
evolutionary development of the labyrinth. From its most elementary type 
m certain primatrve fish forms, the labyrinth, then embracing only a 
momentary vestibular apparatus, is gradually evolved, finally reaching 
m the more highly organized fishes the most highly developed and complex 
foim of vestibular mechanis m. Only with the appearance of the amphibia 

10 Pritchard: Fixation of Stapes, Trans. U to l Society United Kingdom, Vol. vii, p. 60. 







Fig. 143.—Horizontal section through oval window (right), dividing stapedial foot-plate, vestibule, 
and basal turn of cochlea. (After Paul Manasse.) 

A, newly formed bone in region of anterior margin of oval window; B, foot-plate of stapes. 

Stapes itself is not involved, nor is the annular ligament destroyed. Stapes is therefore not anky- 
Josed. Coincidently there is complete atrophy of Corti’s organ. 









Fig. 144.—Horizontal section through stapes, and basal turn of cochlea. (After Paul Manasse.) 

The characteristic bone changes are seen in the foot-plate of the stapes, extending thence in front 
of anterior border of oval window through the entire thickness of the cochlear capsule to its inner per¬ 
iosteal lining. 

The posterior end of the stapedial foot-plate is enormously thickened by the outgrowth of the new 
bone and the annular ligament is destroyed, giving rise at this point to complete osseous ankylosis. 
At the anterior margin of the oval window, the annular ligament, though bounded on either side bv 
newly formed bone, still persists. 

The auditory nerve and spiral ganglion are atrophied. 





GRAY’S THEORY 


247 


does the adjunct mechanism ol hearing, the cochlea, begin to appear. From 
this we see that the vestibular and semicircular canal system is older by 
untold ages than the cochlear mechanism. This fact, as will be shown 
later, may be not without bearing upon the pathogenesis of otosclerosis. 

Gray 11 regards otosclerosis as a degenerative process, in which evi¬ 
dences of inflammatory changes, past or present, are completely absent. 
It is, moreover, according to Gray s view, a degenerative process dependent 
upon certain inherent defects in the bone cells or bone structure of the 
organ of hearing. Regarding such structural defects or errors as develop¬ 
mental variations, and recalling that such variations are particularly prone 
to involve structuies of comparatively recent biological descent, we are 
provided with a hypothesis by which to explain the frequency of sclerotic 
changes in the cochlea, and their comparative rarity in the structures of 
the vestibular mechanism. 

Gray apparently believes that these biologic or developmental defects 
in the labyrinthine capsule play a major part in the prevalence of the 
disease. If the developmental defects are sufficiently pronounced, the 
individual is not likely to escape otosclerosis; if they are completely absent, 
no exciting cause will induce the disease; between these two extremes are 
individuals who may or may not escape the disease, and in whom inter¬ 
current conditions e.g., acute otitis media, toxic agents in the blood, 
syphylis, etc.—may be the deciding factor. 

With Dr. Gray’s view as to the incidence of the disease, Dr. J. S. 
Fraser seems not to be in complete accord in that he apparently believes 
that an exciting cause of extra-labyrinthine origin is necessary to its incep¬ 
tion; and among such causes he gives acute inflammatory lesions of the 
middle ear a very important place. This view, whether accepted in whole 
or part, calls for serious consideration, on account of its important bearing 
upon the question of prevention or prophylaxis. 

That the process is one of absorption of the normal bone and its replace¬ 
ment by new spongy bone, rather than rarefaction or spongification of the 
old bone, is clearly shown by the accompanying illustrations (Figs. 143, 
144, 145). Two of them represent cases of otosclerotic stapedial ankylosis. 
In each it is seen that the new spongy bone occupies not only the position 
of a previously existing normal structure, but extends far beyond its 
normal limits. It is clear, therefore, that the lesion may give rise to exos¬ 
toses from different parts of the bony capsule. These growths may pro¬ 
trude externally from some aspect of the promontory encroaching upon the 
tympanic space, or internally into the vestibulum. Extending from one or 
both walls of the oval niche, this recess may be so narrowed as to lock the 
stapes in an immovable grip. Or the cartilage covering the foot-plate 
of the stapes may be absorbed, and its place occupied by a bony growth 
extending into the vestibular cavity (Fig. 144). Obviously stapedial fixa¬ 
tion may be produced in two ways,— i.e., (1) by osseous union to the 

11 Gray: Otosclerosis; H. K. Lewis & Co., London, 1917. Gray: Otosclerosis; 
Review of J. S. Fraser: Journal of Laryng. and Otol., Vol. XXXIII, p. 16. 



248 


OTOSCLEROSIS 


margins of the oval window, and (2) by pressure of bony growths from 
other parts of the labyrinthine capsule (Fig. 143). Politzer has recorded 
a case in which, in addition to characteristic changes involving the stapes 
and oval window, the scala vestibuli was completely filled by compact 
bone. Contemplation of the character of the lesion is enough to convince 
one of the futility of local treatment. 

The causes and conditions which inaugurate these changes are still a 
fruitful subject of investigation. Siebenmann’s investigations led him to 
believe, as Gray now holds, that otosclerosis is a developmental abnor¬ 
mality rather than a disease in the ordinary sense. He regards it as a last 
stage in the process of the development of the labyrinthine capsule,—a 
stage which ordinarily does not take place. He believes that the process ori¬ 
ginates not in the bon}^ capsule, but in the layer of cartilage-cells lying be¬ 
tween the original membranous capsule of fetal life and the surrounding 
bony capsule later developed from the connective tissue of the skull. Ac¬ 
cording to this view, otosclerosis is in reality a process which, while abnor¬ 
mal in the labyrinthine capsule, is the rule in the other bones. To under¬ 
stand this theory we must remember that the bony labyrinth attains 
approximately its maximum size at birth. This, of course, is the reverse con¬ 
dition to that governing the other bones of the skeleton, which from birth to 
maturity must constantly increase in size while maintaining their presribed 
form.This process of growth is accompanied by a continual loss and regen¬ 
eration of tissue. Similar changes occurring in the fixed and closely confined 
bony labyrinth cannot fail to result in distortion or obliteration of normal 
structures. Siebenmann’s theory, while never generally accepted, seems to 
have commanded the respect of Korner and many other distinguished 
students of otology. 

Apparently we are on the threshold of a period of renewed interest 
and activity—at least throughout the Anglo-Saxon world of otologists— 
in the study of the causes and pathogenesis of this at present rather hope¬ 
less disease. Unfortunately the enormous amount of work which in the 
past has been focused upon the pathology of otosclerosis, has yielded 
results of academic interest, rather than of practical value to suffering 
humanity. We know (something of) the histologic character of the lesion, 
and we are provided with fairly convincing theories as to the pathogenesis; 
but as to treatment or prevention we have only hypothesis based for the 
most part on pure conjecture. There is nothing in the way of evidence 
that any causal relation exists between tympanic lesions, inflammatory or 
suppurative, and the characteristic bone changes of otosclerosis. While 
such hypothesis may furnish useful bases for a perfectly justifiable empir¬ 
icism, they may never-the-less be misleading and may involve the dis¬ 
advantage of retarding work in a direction of effort to establish a more 
solid basis for treatment, preventive or corrective. In the solid work of 
Gray, Siebenmann, Manasse, Korner and others we have the ground work 
for the next advance. 



GRAY’S THEORY AS TO PATHOGENESIS 249 

A more recent hypothesis is that advanced by Gray, of Glasgow, 11 
who connects the lesion with failure of the local blood supply, and in this 
way brings it into some etiological relation with depressed systemic con¬ 
ditions, and particularly with those in which anaemia is a prominent feature. 


Fig. 145. —Horizontal section through right oval window. (After Paul Manasse.) 

Widespread and characteristic bone changes are seen involving the foot-plate of the stapes, the 
entire thickness of the cochlear capsule, and the outer wall of the vestibule. 'Ihe more lightly stained 
areas represent the changes of long standing, the dark areas the more recent proliferation of new bone. 

Total destruction of annular ligament and complete osseous ankylosis of stapedial foot-plate are 
seen at posterior margin of oval window; the same process, though in a less advanced stage, being in 
evidence at the anterior margin of the oval window. 

The membranous labyrinth and both branches of the auditory nerve are atrophied. 

In support of this view, Gray marshals the following facts: (1) the well 
recognized absence of any evidences of inflammatory action; (2) the char¬ 
acter of the initial change,— i.e., absorption of bone and cartilage through¬ 
out small circumscribed areas of bone, which are differentiated by 


11 Gray: Transact. Otol. Soc. United Kingdom, vol. vii, pp. 76-79 







250 


OTOSCLEROSIS 


well-marked lines of demarcation from surrounding healthy bone; (3) the 
deposition of new spongy bone to replace the structures which have been 
absorbed; (4) the fact that this absorption without inflammatory reaction 
and the subsequent replacement by spongy bone are what might be ex¬ 
pected in a tissue in which the local blood supply had failed; (5) the charac¬ 
ter of arteries supplying bone,— i.e., that of vessels incapable of changes 
in calibre in response to variation in arterial force; and, finally, (6) the 
anatomical peculiarities of the bony capsule,— i.e., very dense bone in 
which the calibre of the Haversian canals is much smaller than in any of 
the other bones of the body. This reduced calibre of the Haversian canals 
increases the friction which the heart action has to overcome. Gray, 
therefore, believes that, when for any reason the arterial force is markedly 
reduced, and particularly if the quality of the blood is pathologically 
changed, the conditions become ripe for stagnation of the blood in the 
vessels traversing the bony capsule, with possibly resulting thrombosis. 
Thrombosis in these minute vessels effectually cuts off the blood supply 
from certain circumscribed areas of bo'ne, in which consequently are 
inaugurated the characteristic changes of the disease. Gray holds that 
this theory explains in part the greater predisposition of women to the 
disease, women being more subject than men to various forms of anaemia. 
It does not, on the other hand, coincide with the strong influence which 
heredity is known to exert upon the incidence of the disease. 

Symptoms and Diagnosis. —All observers agree that a perfectly 
uncomplicated case of otoslcerosis, with bone changes confined to the 
stapedio-vestibular region, is easily diagnosticated. There are in the main 
but two varieties of the disease which present special difficulties of diag¬ 
nosis,—namely: (1) otosclerosis with foci of disease so distributed as to 
involve directly the cochlear structures, and (2) otosclerosis complicated 
by chronic catarrhal otitis media. We shall begin, therefore, with the 
symptoms which characterize the lesion in the most uncomplicated form, 
viz., otosclerosis with deafness dependent upon fixation of the stapes. 

History. In characteristic cases there is usually a history of very 
gradual development of symptoms. Frequently there are no intercur¬ 
rent diseases or disorders with which the patient associates his aural 
complaint. If the lesion is advanced, both ears are almost invariably 
involved. According to Bezold, the lesion is bilateral in 88 per cent, of 
cases. In the early stages, however, evidences of the disease may be con¬ 
fined to one ear. Frequently the ear in which symptoms appear last is 
the one in which the progress of the lesion is subsequently most rapid and 
the deafness or impairment most pronounced. The history may be abso¬ 
lutely negative as to catarrhal or suppurative conditions having involved 
the tympanic cavities. In a word, there may be no account of any con¬ 
ditions within the nose or nasopharynx, or in the Eustachian tubes, with 
which the aural lesion can be in any way associated. 

Symptoms— The patient usually complains of two symptoms,—namely, 
impaired hearing and tinnitus aurium. Either one may be the first to 


SYMPTOMS: BEZOLD'S SYMPTOM COMPLEX 


251 


attract his attention, though impairment of hearing is probably always 
the first symptom. It is conceivable that an adventitious subjective sound 
might disturb the patient while moderate recession of the normal hearing 
power might escape his notice. This probably explains the occasional 
statement that tinnitus was present long before the hearing became 
impaired. 

Deafness .—The impairment of hearing is frequently so gradual in 
its advance as to be fairly pronounced before the patient is fully aware 
of his functional loss. In the early stages the impairment of hearing may 
be manifested by slight loss of auditory acuteness for the watch, acoumeter, 
and the conversational voice, and by very slight increase in hearing by 
bone conduction. Thus, the sound of a vibrating tuning-fork in contact 
with the mid-line of the skull may seem louder in the ear first affected, or 
in the one in which the lesion is more firmly implanted. 

In advanced stages of the disease, the hearing tests give the following 
fairly definite reaction: The hearing distances for the watch, the acou¬ 
meter, and for the whisper and conversational voice are very considerably 
reduced. The lower tone limit is always elevated, and loss of hearing for 
progressively higher tones in the musical scale usually advances with the 
progress of the lesion. The perception of the higher musical tones is, on 
the other hand, well maintained, and the upper tone limit may be abso¬ 
lutely normal. The period of hearing by bone conduction is always defi¬ 
nitely, and usually very considerably, prolonged. 

This brings us to Bezold’s triad symptom complex,—viz., (a) loss of 
hearing for the lower musical tones, (b) prolonged period of hearing by 
bone conduction, and (c) negative Rinne. Bezold claimed that the pres¬ 
ence of this syndrome, in cases presenting no evidences either of tympanic 
disease or of disease of the auditory nerve, could be positively relied upon 
as pointing to otosclerosis with stapedial fixation. 

As a corroborative measure, Gelle’s test should be applied. If conden¬ 
sation of the air in the auditory meatus exerts no influence upon the 
intensity with which sound is heard through the cranial bones, the diag¬ 
nosis of stapedial fixation is strongly confirmed. 

Tinnitus Aurium .—There is no aural disease in which the subjective 
sounds are more constant or persistent. Fortunately, there are many 
cases in which the patient is apparently not greatly disturbed by them, 
either by reason of their moderate intensity or from the fact that custom 
and possibly a strong will enable him to ignore them. In other cases the 
head noises are the most distressing feature of the disease, sometimes 
rendering life a burden. Unlike the impairment of hearing, the head 
noises are, fortunately, subject to periods of comparative amelioration, or 
at least to periods during which the patient is less disturbed by them. 
There is, however, no promise that they will disappear as the disease 
advances; and if the lesion is confined to the region of the oval window, 
they are not unlikely to increase as the hearing power recedes. This, in 
the writer’s opinion, constitutes one of the most alarming possibilities of 


25 2 


OTOSCLEROSIS 


this dreadful disease,—a possibility which with nervous or mentally 
unstable individuals may far outweigh the serious one of prospective loss 
of hearing. 

Vertigo .—While vertigo is not a particularly prominent feature of the 
disease, moderate dizziness is complained of in a certain proportion of 
cases (22 per cent., Bezold). It usually does not amount to more than 
slight subjective vertigo, lasting but a few moments. In others, it assumes 
so severe a character as to overbalance all other symptoms, and to justify 
even the most drastic surgical measures for its relief (Lake). 

Paracusis Willisii .—This condition has already been described as an 
occasional symptom of hyperplastic otitis media with fibrous fixation of 
the stapes. It is a much more frequent phenomenon of otosclerosis unac¬ 
companied by disease of the auditory nerve. 

The next step is the examination of the ears both by inspection and 
by catheter inflation. Inflation usually reveals a tube of normal calibre, 
and is practically without influence upon the deafness,— i.e., no note¬ 
worthy improvement results as in the case of chronic catarrhal otitis 
media. This is an important diagnostic point. If, in addition to this, the 
drum membranes are seen to occupy approximately their normal position 
and to present no changes characteristic of chronic middle-ear disease, 
the diagnosis of otosclerosis may be regarded as proved. 

There is one physical sign which is regarded as more or less strongly 
indicative of otosclerosis,—viz., the presence of a reddish or pink blush, 
seen upon, or rather through, the membrana tensa, usually behind the 
umbo (Schwartze). It is in many cases absent. When present it is sup¬ 
posed to be due to congestion of the mucous membrane covering the 
promontory, secondary to pathological changes in the bone beneath. 

Before leaving this subject the writer wishes to revert for a moment to 
a consideration of Bezold’s syndrome,—viz., prolonged hearing by bone 
conduction, elevation of the lower tone limit, and reversed ratio between 
hearing by air conduction and bone conduction. This combination is 
present also in any tympanic lesion giving rise to stapedial ankylosis. It is, 
therefore, of special value as pointing to otosclerosis only in cases in which 
tympanic disease can be definitely excluded. Since disease of the auditory 
nerve regularly results in reduction of hearing by bone conduction, Bezold’s 
syndrome must be lost or changed whenever the lesion involves the cochlear 
filaments of the nerve. It is, therefore, of considerable value in determin¬ 
ing w hether the lesion is confined to the stapedio-vestibular region or is so 
distributed as to involve also the cochlea. 

7 o epitomize. The characteristic features of the disease may be summed 
up as follows: History of hereditary predisposition (frequently obtain¬ 
able); history of very gradual, but progressive, bilateral impairment of 
hearing, not subject to marked variations in response to external condi¬ 
tions; tinnitus present and usually persistent; paracusis present; absence 
of physical signs of chronic tympanic disease; patent Eustachian tubes; 
catheter inflation followed by little or no real functional gain. Deafness 


SYMPTOMS: HARTMANN’S DIFFERENTIAL TEST 


253 


characterized by auditory failure for low musical tones, upper tone limit 
remaining normal or nearly so; bone conduction increased; Rinne negative. 
Intensity of sound as conveyed through the cranial bones uninfluenced by 
compression of air in auditory meatus (Gelle). With such a picture the 
physician who fails to recognize otosclerosis with stapedial fixation is 
certainly not a practical otologist. 

Otosclerosis with Involvement of the Cochlea.— In describing the 
pathology of otosclerosis, it was pointed out that the disease may attack 
an y portion of the labyrinthine capsule; and that while the region of 
predilection is found in the immediate neighborhood of the stapedio- 
vestibular articulation, the lesion may be so distributed as also to involve 
the intracochlear structures. In this way may be inaugurated changes 
affecting the cochlear nerve filaments, leading to many of the symptoms 
characteristic of a primary nerve lesion. Obviously such extension of the 
disease must produce some modification of the clinical picture. 

Symptoms.— For emphasis and comparison, let us consider first a case 
of otosclerosis with extensive involvement of the cochlea and in which 
fixation of the stapes has not taken place. As in the type first described, 
the patient usually complains of impaired hearing in both ears, and sub¬ 
jective noises. The deafness is at first very gradual in its advance, but 
later may be subject to very marked periodical changes for the worse,— 
i.e., loss of hearing which is never thereafter regained. The tinnitus is 
usually a distressing symptom. It may be very persistent, or may become 
less severe with the progress of the disease, finally subsiding as the patient 
approaches absolute deafness. This, however, is not invariable, cases 
having been recorded in which patients have become absolutely deaf yet 
continued to suffer from the most distressing head noises. Paracusis 
Willisii is not present. There may be no history of past or present tym¬ 
panic lesions having any etiological relation to the disease. 

Examination of the ears reveals comparatively normal drum mem¬ 
branes,— i.e., drum membranes fairly normal in position and showing no 
marked structural changes. The characteristic red “ blush ” behind the 
umbo may or may not be present. The Eustachian tubes are patent, and 
catheter inflation exerts no influence on the hearing. 

Deafness .—In advanced stages the hearing tests show the following 
characteristic changes: The lower musical tones may be well perceived 
and the lower tone limit but little changed or practically normal. The 
upper tone limit is lowered, and all the higher tones are heard with re¬ 
duced intensity. The period of hearing by bone conduction is reduced, 
and Rinne remains positive or normal. Bezold’s triad syndrome is there¬ 
fore absent. 

Hartmann's Differential Point .—A rather striking differential test, 
based upon the normal hearing periods for the different tuning-forks by 
aerial conduction, was first announced by Ed. Hartmann. He found in 
lesions involving the cochlear nerve not only that the higher tuning-forks 
were heard during a much shortened period, but also that the relative 


254 


OTOSCLEROSIS 


curtailment as compared with the normal hearing periods become progres¬ 
sively more marked as we ascend in the musical scale. Exactly the reverse 
is the case with otosclerosis confined to the stapedio-vestibular region. 
The experiment may be stated briefly as follows: In otosclerosis confined 
to the stapedio-vestibular structures, the hearing periods are greatly 
reduced for the low musical tones, but gradually approach the normal as 
we ascend in the musical scale. In otosclerosis with involvement of the 
cochlear nerve (the stapes remaining mobile), the hearing periods are 
progressively reduced as we ascend from the lower to the upper end of the 
musical scale. 

In the above we have taken two extreme types of the disease in order 
•• to bring out more clearly and graphically the clinical features character¬ 
istic of stapedial ankylosis on the one hand, and disturbance of the coch¬ 
lear nerve on the other. In a majority of cases, however, in which post¬ 
mortem findings have demonstrated the presence of intracochlear disease, 
there have been coincident changes in the region of the oval window result¬ 
ing in fixation of the stapes. It is clear, therefore, that we shall find in 
many cases functional reactions characteristic both of stapes ankylosis 
and of disease of the cochlear nerve. Thus, both upper and lower tone 
limits may be curtailed, and the tendency to increase in bone conduction 
commonly resulting from stapedial fixation may be counteracted by the 
cochlear lesion. With such contradictory reactions, it may be difficult to 
differentiate between otosclerosis and a lesion primarily involving the 
cochlear branch of the auditory nerve. As bearing upon such a problem, a 
possible history of heredity, a history of gradual bilateral onset, and the 
determination by functional tests of greater disturbance of hearing for 
the lower musical tones than would ordinarily result from a primary nerve 
lesion, may aid us in reaching a correct diagnosis. 

The course of the disease varies greatly in different cases. In some 
cases the disease progresses rapidly from the start, leading within a com¬ 
paratively short period to very marked—sometimes to profound—deafness. 
Such rapid advance in the lesion and its resulting deafness has been ob¬ 
served to occur with greater frequency in patients suffering also from 
constitutional syphilis. Politzer states that women suffering from oto¬ 
sclerosis often show a considerable permanent increase in the deafness with 
each childbirth. When, without intercurrent constitutional disease, the aural 
disease runs a particularly rapid course, the inference seems admissible 
that the lesion is so distributed as to involve early the perceptive mecha¬ 
nism proper. Fortunately, there is a large class of cases in which the disease 
is very gradual in its advance. In some cases years may elapse without 
apparent progress in the lesion. To this extent, however, the prognosis 
is always bad, namely, that individuals in whom the lesion has produced 
marked impairment by middle life will probably in old age reach a very 
distressing grade of deafness. The most hopeful prognosis belongs to those 
cases in which the disease develops late in life, or rather in which the func¬ 
tional disturbance then demonstrable is of moderate grade. Such a case 



TREATMENT 


255 


may be so gradual in its advance as to bring the patient to old age without 
disabling deafness. 

Otosclerosis Complicated by Chronic Catarrhal Otitis Media._ 

W hen chronic catarrhal otitis media coexists with otosclerosis, the one 
lesion may so obscure the other that a positive diagnosis of the two condi¬ 
tions can not be made. Certainly such a diagnosis is quite impossible as 
a result of a single examination, no matter how careful this examination 
may be. As pointing to otosclerosis we may in some cases have the fol¬ 
lowing somewhat indefinite facts,—viz., (1) the deafness may be more 
pronounced than would be expected from the tympanic lesion alone, and 
(2) local treatment may exert less influence upon the symptoms than would 
be expected in uncomplicated tympanic disease. With well-marked 
evidences of tympanic disease the early stages of otosclerosis can not be 
diagnosticated. 

The opinion expressed by Whiting, that profound deafness is always 
due to labyrinthine or nerve disease, is a belief probably subconsciously 
held by most otologists. W r ith respect to tympanic disease, there is a 
degree of deafness which probably is never reached unless the movements 
of the stapes within the oval niche or window are mechanically restrained. 
Personally, I believe that a reversed Rinne always means stapes fixation. 
But with the physical evidences of chronic non-suppurative tympanic 
disease, whether a negative Rinne points to fibrous immobilization or to 
osseous union resulting from otosclerosis, is a question which is not alwavs 
soluble. 

Treatment. —If we accept Siebenmann’s theory that the disease is 
simply an abnormal stage of development, all treatment seems useless. 
If we agree with Gray that the disease may be in some degree dependent 
upon depressed systemic conditions giving rise to anaemia, the prospect 
seems more favorable. In its most typical form,— i.e., otosclerosis without 
evidences of tympanic disease,—I can see no possible influence which local 
therapeutic measures can exert upon the progress of the lesion. The 
occasional statements of well-known otologists as to cases of otosclerosis 
which have responded favorably to local treatment are probably to be 
regarded as cases of mistaken diagnosis. Such experiences are not, how¬ 
ever, to be altogether ignored, since they serve to emphasize two facts,— 
viz., (!) that cases of deafness apparently traceable to otosclerosis are 
sometimes on further investigation found to be cases of temporary deafness 
dependent upon transient causes, which yield readily to local treatment; 
and (2) that the deafness of otosclerosis is sometimes markedly increased 
by certain obscure but transient conditions within the tympanum, such 
cases showing rapid improvement as a result of local treatment. As 
illustrating the class just referred to may be mentioned the following ex¬ 
perience of the writer: A patient referred to him by another physician 
gave a history of slight impairment of hearing of two or three years’ stand¬ 
ing which had recently become very marked in the left ear. Both drum 
membranes were practically normal in appearance. Functional tests showed 


256 


OTOSCLEROSIS 


in the left ear a type of partial deafness characteristic of disturbed sound 
conduction. Little or no improvement resulted from the first inflation. 
As a result of these findings a tentative diagnosis of otosclerosis was made, 
the patient being advised to submit to a short course of treatment in order 
to prove definitely the character of the disease. To the writer’s surprise, 
the hearing very rapidly improved under the plan of treatment usually 
employed in chronic catarrhal otitis media, soon reaching a degree of acute¬ 
ness which, though slightly below the normal standard, might be regarded 
as little more than the physiological impairment due to his fifty-five years. 
In this case the writer did not flatter himself that he had relieved a case 
of otosclerosis, but rather that he had relieved some transient condi¬ 
tion within the tympanum, the nature of which he had not been able to 
determine. 

Leaving such exceptional cases out of our consideration, we must come 
back to the regrettable fact that otosclerosis is a lesion which ordinarily 
is not helped by local treatment of any kind. Catheter inflation usually 
reveals open tubes and to some extent exercises the drum membranes, but 
can have no influence upon the progress of the disease. Politzer states 
that vibratory massage through the external auditory meatus is of value 
in the early stages of the disease,— i.e ., before osseous union between the 
foot-plate of the stapes and margin of the oval window has taken place. 
He also recommends the administration of iodide of potassium in 5-grain 
doses three times a day, this to be continued through 25 or 30 days, and 
to be repeated two or three times during the year. Politzer believes that 
this periodic use of the iodides helps in beginning otosclerosis to stay the 
progress of the disease. 

Siebenmann advocated small doses of phosphorus, to be given more or 
less continuously over a period of years. It is worthy of note that neither 
the iodide of potassium nor the phosphorus was expected to result in 
improvement of hearing, but simply to retard the progress of the disease. 
Couple this fact with the statement of Bezold that a large number of cases 
become stationary with only moderate impairment of hearing, and we 
have a commentary on the difficulty of determining the real value of these 
or other drugs in this disease. 

While otosclerosis is a disease for which local treatment promises little, 
there is much that can be done for such a patient. In the first place, we 
are able in many cases to assure him that his deafness will in all probability 
be very gradually progressive, and that it may never reach a degree inter¬ 
fering seriously with his usefulness. There is no question that much need¬ 
less suffering has been caused in certain cases by a frankly unfavorable 
prognosis, the correctness of which has been disproved by subsequent 
events. The writer has under his care a patient for whom another aurist 
eight years ago predicted rapidly progressive loss of hearing. And yet 
during the past eight years this man’s hearing has not changed demon¬ 
strably for the worse, and during this period he has been able to accomplish 
a very considerable amount of useful work. I believe, therefore, that when 


TREATMENT 


• 257 


the heaiing is only moderately impaired, we should acquaint the patient 
with the natuie of the lesion only to the extent of making him appreciate 
the importance of carrying out such general provisions as may seem best 
foi him, and that their neglect carries distinct danger of serious deafness. 

riiere is probably no disease in which hygienic measures and a wise 
regulation of the patient’s mode of life are of more importance than in 
otosclerosis. This view seems admissible when we consider the following 
facts. It is known that constitutional syphilis, if not a cause of the disease, 
is at least a factor influencing its rapid advance; that anaemia influences 
its progress, that with women the onset of the disease seems frequently to 
be associated with the age at which they are most subject to chlorosis; 
that women suffering from otosclerosis commonly show a definite advance 
of the lesion, as evidenced by permanent increase in deafness, after each 
childbirth. Presumably these conditions influence the disease either 
through lowered vitality or through the anaemia which is their common 
characteristic. If these depressed constitutional conditions hasten its 
advance, it seems a logical deduction that by the reverse process, of build¬ 
ing the patient up to his maximum of physical health, we may to some 
extent hold the disease in abeyance. 

In the section dealing with the etiology, reference is made to tonsillar 
infection as a possible and probable factor in the incidence of certain cases 
of the disease. Naturally if such a causal relationship could be established 
in any large series of cases, the importance of tonsillectomy in the control 
of the disease would be evident. There is at hand no data justifying any 
statement more definite than that the tonsils should be carefully studied in 
the early stages of all cases of otosclerosis. Three cases reported by Mr. 
Richard Lake of London are of sufficient interest to justify their inclusion 
in brief outline here. 12 

Case I. Was that of a young woman, oet. 24, who presented characteristic 
symptoms of otosclerosis. Removal of the tonsils brought marked im¬ 
provement, both in the hearing and as to the physical appearance of the 
drum-membranes. A relapse was traced to an infected maxillary sinus, 
disinfection and treatment of which resulted once more in marked 
auditory gain. 

Case II. “Women, aged about 25, with recent history of rapidly in¬ 
creasing deafness; both ears showed red reflex. Tonsils removed without 
delay. Two weeks later, redness of fundi gone and hearing as good 
as ever. ” 

Case III. Woman of thirty years, suffered from deafness diagnosti¬ 
cated as due to otosclerosis. Treatment by various methods resulted only 
in moderate and temporary improvement in hearing. Finally the tonsils 
were removed, with a gain in hearing which up to the time of the report 
had been maintained. 

There is no doubt that overwork, mental or physical, the strain of busi¬ 
ness anxieties, excessive confinement to business, unrelieved by regular 
hours of exercise in the open air, may unfavorably influence the disease. As 

12 Richard Lake: Journal of Otology and Laryngology, vol. XXXVII, 1922, p. 301. 




258 


OTOSCLEROSIS 


nearly as the individual's circumstances admit, it should be insisted upon, 
therefore, that his business activities be brought within reasonable limits, 
and he should be made to understand that any indulgence in such business 
excesses may in the end be paid for dearly by serious loss of hearing. 

Tobacco and alcohol, when they influence the hearing injuriously, do so 
chiefly through their action upon the auditory nerve. It is clear, therefore, 
that excessive smoking or drinking may have disastrous results in a lesion 
in which the end organs of the nerve may be maintining their function 
under conditions which have already become abnormal. Tobacco and 
alcohol should, therefore, be indulged in only with the greatest moderation. 

Drugs, other than such tonics as may be occasionally indicated, have 
little or no specific value in otosclerosis. The patient should be instructed 
that quinine, the salicylates, and most of the coal-tar derivatives induce 
intra-labyrinthine congestion, and are under ordinary conditions distinctly 
contra-indicated. 

Gray places great emphasis upon the importance of combating anaemia 
in any form; and it may be that periodic blood examinations—particularly 
young women suffering from otosclerosis—might suggest measures which 
would prove of value in maintaining these patients in the best condition 
or combating the advance of the aural lesion. 

Dr. J. A. btucky of Lexington, Kentucky, believes an important factor 
in the progress, if not in the causation, of otosclerosis to be the circulation 
in the blood of toxins resulting from errors of diet. He has recorded his 
experience with a series of cases which he has had under observation during 
many yeais, and in which he is convinced that systemic care in preventing 
this form of auto-intoxication has played an important role in staying 
the progress of the disease. 

The patient should be seen from time to time, and the hearing retested in 
order to determine the progress or the comparative quiescence of the lesion. 
It is of course particularly important that any catarrhal condition within 
the tubes or tympanic cavities should have prompt and efficient treatment. 

The plan above outlined suggests in a general way what seems to the 
writer the best way of caring for these patients. While active local treat¬ 
ment is, as a rule, not indicated, it is important that the patient should 
considei himself constantly under the care of a competent aurist. By 
this is meant that he should return at stated intervals for examination 
and advice. This shifts the responsibility of his condition from his own 
shoulders, and, what is of considerable importance in these cases, elimi¬ 
nates the risk of much useless and possibly harmful treatment by ignorant 
or unscrupulous practitioners. 

In what has been said above, the writer has had in mind the rather 
arge class of cases in which the hearing is only moderately impaired the 
lesion being apparently quiescent or verv slowly progressive' 

There is, unfortunately, another class of patients,— i.e., those whose 
deafness is either progressing rapidly from bad to worse, or whose hear¬ 
ing is already so far lost as to render conversation exceedingly difficult 
or impossible. Such patients should be told frankly of the incurable nature 


SURGICAL TREATMENT OF DEAFNESS 


259 


of their disease, and encouraged to make use of artificial aids to hearing. 
The very best advice that can be given to such a patient is that he apply 
himself diligently under the advice of a competent teacher to the task of 
acquiring the art of lip-reading. Only in this way can he rob his infirmity 
of its most unbeaiable haidship, -that of practical isolation among 
his fellows. 

Surgical Measures for the Relief of Deafness .—Before leaving this sub¬ 
ject, a woid must be said as to the various surgical measures which have 
been pi oposed fi om time to time with the purpose of relieving ossicular 
ankylosis and thereby improving the hearing. They may be mentioned 
in the following order: 

1. Mobilization of the stapes by passive movements by means of 
instiuments intioduced through a window in the drum membrane. The 
best opening is secuied by a horseshoe-shaped incision in the postero- 
superior quandrant (Fig. 146). 

The flap of drum membrane 
thus formed is then folded 
downward, leaving the incudo- 
stapedial articulation in view 
and accessible to instruments. 

The head of the stapes is then 
gently moved in different direc¬ 
tions as far as its attachment 
to the lenticular process of 
the incus will allow without 

danger of injury to the annular Fia - 146 — Diagrams showing line of incision, and the 

° , r 1- J- i j • resulting flap, deflected. 

ligament or ot disarticulation 

from the incus. The results of this procedure have not given it a per¬ 
manent place in aural therapy. 

2. Reduction of abnormal ossicular tension by division of the tendons 
of the tensor tympani and stapedius muscles. The fact that this operation 
has no champion among recognized authorities points to the disappoint¬ 
ing results obtained. 

3. Division of fibrous bands binding the crura of the stapes to the walls 
of the oval niche. Politzer makes the point that this operation, while 
without proved value in the fibrous fixation of chronic catarrhal otitis 
media, is in certain cases quite successful in the fibrous ankylosis follow¬ 
ing suppurative otitis media. 

4. Removal of membrana tensa, malleus, and incus,—the stapes being 
left in situ. This procedure was based upon the hypothesis that the drum 
membrane, malleus, and incus, when incapacitated by disease for the 
function of sound conduction, should be removed in order that the stapes, 
acting alone, may be permitted to receive directly the sound waves from 
without and transmit them to the inner ear. The ultimate results of this 
operation proved so disastrous to the auditory function, that it has no 
advocates among the otologists of to-day. These operations, mentioned 
for their place in otological history, are quite obsolete today. 









CHAPTER X. 

THE ANATOMY AND PHYSIOLOGY OF THE LABYRINTH. 

The inner ear, or labyrinth, embraces two distinct mechanisms,—viz., 
the cochlea , or essential organ of hearing, and the vestibular apparatus 
(saccule, utricle, and three semicircular canals), a contributory organ of 
equilibrium or orientation. These structures are contained within a series 
of little communicating cavities in the petrous portion of the temporal 
bone, known as the osseous labyrinth. Within the cavities of the bony 
labyrinth and surrounded by a supporting fluid, the perilymph, are the 
essential structures known as the membranous labyrinth. The inner cavities 
of the membranous labyrinth also contain a fluid which, to distinguish it 
from the surrounding perilymph, is called the endolymph. In form the 
membranous labyrinth follows rather closely the contour of the bony 
spaces in which it is contained. 

Anatomically the labyrinth is separable into three main portions,— 
viz., a central cavity, the vestibule; an anterior portion, the cochlea; and 
a posterior superior portion, the semicircular canals. The vestibule lies 
just internal to the tympanum, with which, but for the foot-plate of the 
stapes, it would communicate by means of the oval window. Anteriorly 
it communicates with the cochlea, and posteriorly with the semicircular 
canals (Figs. 147 and 148). 




Fig. 147.—Bony capsule of labyrinth. 

Fig. 148.—Drawn from metal cast of labyrinthine cavity, a, three semicircular canals- 
b, vestibule; c, cochlea. 

The Osseous Labyrinth. —The cochlea consists of a bony tube 
measuring about l l A inches in length, and coiled two and a half times about 
a central rod or cone into a form somewhat resembling a snail-shell. The 
diameter of the tube near its opening into the vestibule is about 2 mm., 
but from this point its calibre rapidly diminishes, so that after the first 
turn the average diameter is not more than 1 mm. The central axis of 
the cochlea— i.e. } from the centre of the base to the apex—lies in the hori¬ 
zontal plane and is directed forward and outward. Passing horizontally 
through the cochlea from base to apex is a central cone-shaped body known 
260 








THE OSSEOUS LABYRINTH 


261 


as the modiolus. The modiolus is really a hollow central cone around which 
the spiral tube of the cochlea is coiled. Passing outward from the modiolus 
into the spiral canal of the cochlea is a lamina of bone called the spiral 
lamina (Fig. 149). The spiral lamina projects only half-way across the 
lumen of the cochlear canal. From its outer edge a delicate and important 
membranous structure, the basilar membrane, passes in the recent state 
to the outer wall of the cochlear canal, completing its division into two 


Lamina spiralis- 


Internal auditory 
meatus' 


Vestibule (roof/ / 
removed) 



/ 


Scala vestibuli 
(in second whorl) 

Tympanic vault 


Mastoid antrum 


Fig. 149.—Horizontal section through internal auditory meatus, cochlea, and vestibule. 


channels,—an inner, communicating with the tympanum through the 
round window, and known as the scala tympani; and an outer, opening 
into the vestibule, the scala vestibuli. 

Note. —In most text-books the scala tympani is spoken of as the lower cochlear 
channel, and the scala vestibuli as the upper space. This method of description prob¬ 
ably arose from the habit of illustrating the subject by diagrams of the cochlea with 
the apex uppermost. This, however, is not only incorrect but confusing to the student, 
whose effort is, and should be, to learn not only the relation of the various labyrinthine 
structures to each other, but also their relation to the various planes of the skull. With 
the head erect, the modiolus, representing the central axis of the cochlea, is not vertical 
but horizontal, and its direction from the vertical anteroposterior plane of the skull is 
horizontally forward and outward. The spiral cochlear tube winds around this hori¬ 
zontal body, and the spiral lamina, projecting vertically into its lumen, must neces¬ 
sarily divide it not into an upper and lower, but rather into an inner (basal) and outer 
(apical) space. This point is made clear by Fig. 150. 










262 


ANATOMY AND PHYSIOLOGY OF LABYRINTH 


The scala tympani and scala vestibuli communicate with each other at 
the apex of the cochlear pyramid through a small opening known as the 
helicotrema. On the floor of the scala tympani, not far from its beginning 
at the round window, is a small opening leading into a short canal, the 
aqucedudus cochlece. This minute channel provides under certain condi¬ 
tions so dangerous a pathway of infection that the student should have a 
clear appreciation of its possible significance in disease. Beginning in the 
floor of the scala tympani near the round window, the osseous canal leads 
inward and slightly downward through the petrous bone to emerge by a 


Scala vestibuli 


Spiral lamina 


Scala tympani —• 


Internal auditory meatus 



— Inner surface of squama 


Head of malleus (in vault) 


__ Space surrounded by three 
semicircular canals 


Fig. 150.—Horizontal sections through modiolus from base to apex (all structures enlarged), x — y, 

line giving direction of anteroposterior axis of skull. 


triangular opening at the outer edge of the jugular foramen. The 
termination of the bony aqueduct is seen, therefore, on the basal surface 
rather than the interior of the skull. But while the bony aqueduct 
terminates at this point, the membranous canal is continued inward 
through the jugular foramen into the cranial cavity and perforates the 
dura to communicate directly with the subarachnoid space (Politzer, 
Schwalbe, A. A. Gray). According to Politzer, colored fluid introduced 
into the subarachnoid space quickly enters the cochlea and vestibule. 
The cochlear aqueduct is sometimes called aqueduct of the perilymph, 
because through it the cochlear perilymph may pass into the sub¬ 
arachnoid space. The important influence of this communication upon 
the possible consequences of a suppurative invasion of the labyrinth is 
obvious. 

The central canal of the modiolus begins in a depression in the anterior 
wall of the internal auditory meatus near its fundus, called the fossa coch- 


















THE VESTIBULE 


263 


learis (Fig. 151), and gives passage to the cochlear branches of the audi¬ 
tory nerve. Surrounding the orifice of the central canal, the base of the 
modiolus (i.e., fossa cochlearis) is perforated by numerous very minute 
foramina, leading into little canals which radiate outward between the bony 
layers, or plates, of the spiral lamina. These little canals receive the 
branches of the cochlear nerve, which in turn perforate the outer (apical) 
plate, or surface, of the osseous spiral lamina, to pass to their distribution 
in the basilar membrane and organ of Corti. 



The Vestibule .—The position of the vestibule in relation to the middle- 
ear cavity is indicated by the fact that the oval window opens into it and 
marks the centre of its outer wall. It measures 5 to 6 mm. in length (i.e., 
from before backward), and approximately 4 mm. each in width and height. 
On the inner vestibular wall, and nearer the anterior than the posterior wall, 
is a slight ridge, approximately vertical in direction, known as the crista 
vestibuli . In front of this ridge is a small circular depression, the recessus 
sphericus , which in the living subject lodges the saccule. Behind the crista 
vestibuli is an elliptical depression, which lodges the upper part of the 
utricle, and is called the recessus ellipticus. 

Openings into the Vestibule (Figs. 151 and 152).—The vestibule presents 
the five openings of the three semicircular canals. Each canal expands 
at one end into a bulbous enlargement known as the ampulla. The am¬ 
pullae of the horizontal and of the anterior vertical canals are situated 
near each other, these canals entering the vestibule through its superior 
wall, or roof, above the oval window (Fig. 151). The ampulla of the pos- 




264 ANATOMY AND PHYSIOLOGY OF LABYRINTH 


terior vertical canal is found in the floor (Fig. 152, a). Behind this— i.e., 
on the posterior wall near the roof—is the opening of the small end of the 
horizontal semicircular canal (c). Further inward— i.e., near the angle 
formed by the junction of the inner and posterior walls with the roof—is 
the common opening of the anterior and posterior vertical canals (6). In 
the anterior and outer corner of the vestibule,— i.e., where the anterior 



Wire passed through small 
opening (x) of horizontal canal (c) 


Ampulla of posterior vertical 
canal, opening in floor (a) 


Wire passed through 
common opening 
'“(x) of the anterior 
and posterior vertical 
canals (6) 


Fig. 152. Labyrinthine vestibule (d) with roof removed. 


and outer walls join the floor,—is the opening into the scala vestibuli. 
Still another minute opening is found on the inner wall of the vestibule 
leading into the aquseductus vestibuli. The crista vestibuli, recessus 
sphericus, and recessus ellipticus are perforated by numerous very minute 
foramina, constituting the so-called maculae crihrosoe. 'They give passage 
to the saccular and utricular branches of the vestibular nerve. 

The semicircular canals are about 1 mm. in diameter, except at their 
ampullae where their calibre is about doubled. With the head erect and 
with chin indrawn, the horizontal, or external, semicircular canal lies very 
nearly in the horizontal plane. The two other canals are both vertical, 
the anterior \ertical canal lying in a vertical plane directed from within 
outward and forward, and the posterior vertical occupying a vertical plane 
at right angles with that of the anterior vertical,— i.e., directed outward 
and backward. It is obvious, therefore, that each canal lies in a plane at 
right angles to the other two (Fig. 153). In every case the ampullar end 
js situated further forward than the small end of the canal. In the case 
of the horizontal and anterior vertical canals this is made evident by a 
glance at any model or prepared specimen. With the posterior vertical 
on the other hand, this fact is demonstrated only by tracing its lower or 
ampullar, end to its opening in the floor of the vestibule, and there com- 
parmg its position with the common opening of the two vertical canals 
^ig. 152). The posterior vertical canal is on a much lower plane than 


THE MEMBRANOUS LABYRINTH 


265 


the anterior vertical (Fig. 153). The anterior vertical canal is, therefore, 
by many authors called the superior vertical canal, the posterior vertical 
being called the inferior vertical canal. Anterior vertical and posterior 
vertical are, however, much more descriptive, and therefore more useful 
terms. 

Juncture of the two 
vertical canals to form 
their common small 
opening into the vesti¬ 
bule 


Bony covering of sig¬ 
moid sinus 

Posterior vertical canal 


Fig. 153.—Relative positions of three semicircular canals. 

The Membranous Labyrinth. —The membranous labyrinth is every¬ 
where partly surrounded by a supporting fluid, the perilymph. I say 
“partly” for the reason that it is in most regions connected at some point 
with the endosteum lining the walls of the osseous labyrinth. Owing to 
this intervening layer of perilymph, the various portions of the membranous 
labyrinth are necessarily much smaller than the bony spaces in which they 
are contained. The membranous semicircular canals, for example, are 
attached to the endosteum along the outer convex wall of the bony canals, 
being separated elsewhere by a considerable amount of perilymph. The 
membranous canals are, therefore, for the most part very much smaller 
than the osseous tubes in which they lie. Only at their ampullae do they 
enlarge sufficiently to fill approximately their expanded bony compart¬ 
ments. Wherever in the labyrinth filaments of the auditory nerve per¬ 
forate the bony capsule to reach the membranous labyrinth, the mem¬ 
branous parts so supplied are attached to the bone surface thus perforated, 
— e.g., the cristae acusticae of the ampullae and maculae acusticae of the 
utricle and saccule. 

The membranous vestibule is found within the central cavity (vestibule) 
of the osseous labyrinth, and is partly surrounded by perilymph. It con¬ 
sists of the saccule and utricle and the vestibular structures by which they 
communicate with other parts of the membranous labyrinth. The saccule 
communicates directly with the scala media of the cochlea (ductus coch- 
learis) and only indirectly with the utricle. The utricle communicates by 
five openings with the three semicircular canals. 






266 


ANATOMY AND PHYSIOLOGY OF LABYRINTH 


The utricle, about 5 mm. in length, is attached to the posterior part of 
the inner wall of the bony vestibule. Its upper half is lodged in the reces- 
sus ellipticus, behind the crista vestibuli. The portion of the utricle 
which rests against the recessus ellipticus is called the recessus utriculi. 
The recessus ellipticus is perforated by numerous small foramina for the 
passage of the utricular branches of the vestibular nerve; and where these 
nerve filaments enter the utricle, its inner wall is greatly thickened so as 
to project somewhat into the cavity of the utricular sac. This thickened 
area is covered by a highly specialized form of neuro-epithelium, and is 
known as the macula acustica of the utricle. 

The cavity of the utricle communicates by five openings with the three 
semicircular canals (Fig, 154). The ampullar ends of the horizontal and 



Saccule 

r 

I 
I 

Crista acustica of the 

anterior vertical canal --J-< 

Crista acustica of the i ' 

horizontal canal 

Utricle -d® 1 ' 1 


Anterior vertica 
semicircular canal 


i- External (horizontal) 
semicircular canal 
— Posterior vertical canal 

Crista acustica of the 
posterior vertical canal 
-Aquseductus vestibuli 


— Saccus endulymphaticus 
Canalis reuniens 


Cochlear canal 
Fig. 154. —Membranous labyrinth (after Schafer). 


anterior vertical canals open into its roof; the ampullar end of the posterior 
vertical perforates the utricular floor, and the small opening of the hori¬ 
zontal canal and common opening of the two vertical canals enter the 
posterior wall. From the lower anterior end of the utricle is given off a 
small membranous tube which passes forward, inward, and downward 
and unites with a similar tube from the saccule to form the aquceductus 
vestibuli. The aqueduct of the vestibule enters a very small opening on 
the inner wall of the bony vestibule, and traverses the bone in a curved 
direction inward and somewhat backward to emerge by a slit-like opening 
upon the posterior surface of the petrous bone, some 7 or 8 mm. behind the 
internal auditory meatus. It here expands into a closed sac, the saccus 
endolymphaticus. The endolymph spaces of the labyrinth do not there¬ 
fore, communicate directly with the cerebrospinal channels or subarach¬ 
noid space. The perilymph of the labyrinth may, on the other hand 

escape through the aquaiductus cochleae to mingle directly with the cerebro- 
spinal fluid. 

• i T ^ e S acc ul e —TYie other membranous compartment of the vestibule 
is lodged in the recessus sphericus, a somewhat circular depression on the 
inner wall of the osseous labyrinth, in front of the crista vestibuli The 
saccule is only partly separated by the crista vestibuli from the utricle, 






THE CRISTiE ACUSTICRE AND MACULAE ACtTSTICvE 


267 


these bodies being in contact above (Schafer), but having no direct 
communication. The recessus sphericus, sometimes called the fovea 
hemispherica , and the anterior surface of the crista vestibuli present 
numerous small perforations through which the saccular branches of 
the vestibular nerve pass. These nerves penetrate the contiguous surface 
of the saccule, and there give rise to pronounced structural changes 
which will be described later. As a result of these localized changes, 
the cavity of the saccule presents a circumscribed bulging of the 
inner wall, known as its macula acustica. Very similar changes are 
found in the ampullae of the three semicircular canals, being there 
spoken of as the cristce acusticai. From the lower part of the saccule 
a minute membranous canal, the caualis reuniens, passes downward 
to enter the scala media of the cochlea just above its closed vestibular 
extremity. Another small membranous tube leaves the lower posterior 
aspect of the saccule and passes downward and backward to unite with 
a similar canal from the utricle. The union of these little canals forms 
the aquceductus vestibuli , already described. The aquceductus vestibuli 
is also spoken of as the aqueduct of the endolymph. The junction of 
the two canals by which it is formed provides the only communication 
between the utricle and saccule. 

The Cristce Acusticce and Maculae Acusticce. —The crista acustica of 
the canals and maculae acusticae of the utricle and saccule are structu¬ 
rally very similar. The crista acustica of each semicircular canal is situated 
in that part of the membranous ampulla which is attached to the outer 
wall of the osseous ampulla,— i.e., 
that aspect of the bony ampulla 
which is continuous with the outer 
convex wall of the bony canal. 

Each crista acustica occurs as a 
transverse elevation or ridge across 

its ampulla (Fig. 155). The macula Fia - 155. —Diagrammatic section of ampullar 

.. .. , 1 • ,, 1 1 end of horizontal semicircular canal showing posi- 

acustica ot the utricle is attached t ion (a) of crista acustica. 

to the posterior surface of the crista 

vestibuli and the recessus ellipticus behind it; that of the saccule is 
attached to the anterior surface of the crista vestibuli, and in front of 
this to the recessus sphericus. Both maculae occur as irregularly round 
or oval elevations which project from the inner walls into the cavities 
of the saccule and utricle respectively. 

In the cristae acusticae and maculae acusticae alike, the following 
layers may be recognized: 1st, an outer layer of loose fibrous tissue which 
receives the blood-vessels and branches of the vestibular nerve; this layer 
is directly connected with the endosteum covering the contiguous bone 
surface; 2d, a clear or nearly transparent structure known as the tunica 
propria; and, 3d, the inner layer, consisting of so-called neuro-epithelium, 
which is made up of the following structures: superficially, a surface layer 
of elongated pear-shaped, or “flask-shaped,” cells, known as the hair-cells 






268 


ANATOMY AND PHYSIOLOGY OF LABYEINTH 


(Fig. 156, a). They are arranged parallel to each other, their long axes 
being at right angles to the free epithelial surface. Their lower rounded 
extremities do not extend downward as far as to the tunica propria. From 
the upper extremities of these cells, hair-like processes project into the 



Fig. 156.—Structures common to the cristse acusticae and maculae acusticae (after Retzius). 
a. Hair-cells; b, supporting cells of Retzius; c, outer fibrous layer; e, nerve-fibres which, before leav¬ 
ing the fibrous layer, lose their medullary sheaths; /, otoliths. 


cavity of the organ of which they form a part,— i.e., ampulla, utricle, or 
saccule. In the cristae acusticae of the ampullae, the processes are covered 
by a gelatinous substance which is spoken of as the cupola. In the maculae 
acusticae of the utricle and saccule, they project into the gelatinous cov¬ 
ering in which are contained the small bodies known as otoliths. Between 
the hair-cells and the tunica propria, and in contact with the latter, are 
elongated nucleated cells known as the fibre-cells of Retzius (Fig. 156, 6). 
They are regarded as supporting structures, analogous in this respect to 
Deiters’s cells in the organ of Corti, the sensory function being credited 
solely to the hair-cells. 

The outer fibrous layer is rich in blood-vessels and receives the branches 
of the vestibular nerve. In it the arteries break up into a network of fine 
branches. The nerve-fibres, as they leave the fibrous layer, lose their 
medullary sheaths, the axis-cylinders being continued upward into the 
epithelial layer, where their branches pass between and in contact with 



































THE MEMBRANOUS COCHLEA 


269 


the cells. They have not, however, been traced into the hair-cells, and the 
exact distribution of their terminal filaments has not yet been determined. 

The structural arrangement above described characterizes both the 
cristae acusticae of the ampullae and the maculae acusticae of the saccule 
and utricle. In the gelatinous substance covering the latter, and in con¬ 
tact with the hair-cells, clusters of minute bodies, known as otoliths, are 
always present. They consist of crystals of carbonate of calcium. Otoliths 
are not regularly found in the cristae acusticae of the ampullae, though 
their occasional presence in small numbers has been observed (Schafer). 

The Membranous Cochlea— It will be remembered that the spiral 
tube of the cochlea is divided by the spiral lamina and basilar membrane 
into two channels, viz., an inner tube, the scala tympani; and an outer, 
known as the scala vestibuli. There remains to be described a third channel' 
the scala media , which contains the organ of Corti, the essential structure in 
the organ of hearing. 

The spiral lamina (Fig. 157, j) is composed of two bony plates between 
which are channels transmitting the branches of the cochlear nerve. In 



the dry or macerated bone, the outer edge of the lamina spiralis presents 
simply a rather sharp edge. In the recent state, however, the outer part is 
covered with a rather thick layer of connective tissue, and presents on 
section a grooved formation, described as suggesting the letter C. The 
lower margin of this groove, which extends further outward toward the 
outer wall of the spiral tube than the upper, gives attachment to the basilar 









270 


ANATOMY AND PHYSIOLOGY OF LABYRINTH 


membrane. It is called the labium tympanicum (h). The upper margin 
is called the labium vestibulare (c), and the groove between the two, the 
spiral groove ( m ). The labium vestibulare, with the thickened surface 
immediately behind it, is called the limbus. The limbus is formed of firm 
connective tissue, which, however, disappears after maceration. The 
limbus gives attachment to the membrana tedoria ( d ). From the upper 
surface of the lamina spiralis, a little behind the attachment of the mem¬ 
brana tectoria, a delicate connective-tissue membrane passes obliquely 
outward to the outer wall of the spiral tube. This is known as Reissner s 
membrane ( b ). It encloses a third channel, triangular in form, and situ¬ 
ated in the outer part of the cochlear tube between the scala vestibuli 
and the scala tympani. This is called the scala media, canal of the cochlea , 
or ductus cochlearis (e). The ductus cochlearis runs through the spiral 
tube from the cochlear base to its apex, and encloses the organ of Corti (/), 
to be described later. Its apical extremity ends in a blind sac which is 
attached to the cupola. The basal or vestibular end also presents a closed 
extremity, though it receives a little above this a small membranous 
canal from the saccule, the canalis reuniens. The ductus cochlearis con¬ 
tains the endolymph of the cochlea, as distinguished from the scala vesti¬ 
buli and scala tympani which contain perilymph. 

The spiral membrane separates the cochlear duct, or canal, from the 
scala tympani. Along the line of its attachment to the outer wall of the 
spiral tube of the cochlea, the lining membrane of the latter is greatly 
thickened so as to present on section a triangular surface. This spiral 
projection or ridge is known as the spiral ligament (g). Structurally the 
spiral membrane consists of a homogeneous substance in which innumerable 
radiating fibres (about 24,000 in all, Retzius) are stretched from the free 
edge of the spiral lamina to the spiral ligament. It is narrowest at the 
basal or vestibular end, from which point it becomes gradually wider, 
reaching its greatest width near the helicotrema. Within the cochlear 
duct (scala media) and resting upon the basilar membrane is the organ of 
Corti (/). 

The Organ of Corti (Fig. 158) occurs as a rather broad elevation or 
ridge resting upon the basilar membrane throughout the entire length of 
the cochlear duct. On cross-section, and under high magnifying power, 
the following structures are observed: Resting directly upon the spiral 
membrane and near its attachment to the lamina spiralis are two striated 
rod-shaped structures, known as the rods of Corti (I.R.C., O.R.C). That 
nearest the limbus is called the inner rod of Corti, and the one external 
to this, the outer rod. Below, as they rest upon the spiral membrane, 
there is a distinct space between them, but above they incline toward each 
other so as to meet at their upper extremities. The inner rod is described 
as resembling the human ulna in form, presenting an upper extremity 
somewhat similar to the head of that bone. The upper end of the outer 
rod is compared to the head of a swan,—the back of the head representing 
the part which fits into the concavity on the upper end of the inner rod, 


THE ORGAN OF CORTI 


271 



and the projecting part, resembling the swan’s bill, being directed back¬ 
ward (Idg. 159). The rods, both inner and outer, are arranged in single 
parallel rows extending throughout the entire length of the organ of Corti, 
and the inner and outer rows enclose between them a triangular space, 
known as Corti’s tunnel (Fig. 158, 

T. C.). Covering the organ of 
Corti on both sides of the rods 
of Corti are the characteristic 
cell-bodies known as the hair- 
cells (I. H. C.. O. H. C.). These 
are somewhat columnar-shaped 
cells, narrow above, expanded 
and rounded below. From their 
upper extremities tufts of hair- 
processes project. There is a 
single row of hair-cells internal 
to the inner rod of Corti and 
four rows external to the outer 
rod. These are known as the 
inner hair-cells and outer hair- 
cells respectively. Beneath the 
hair-cells, and between them 
and the basilar membrane, are 
a number of supporting cells of 
very different type, known as 
Deiters’s cells. These cells are 
cylindrical below and rest directly 
on the basilar membrane. Above 
they become narrowed, each into 
a slender process which extends 
upward between the hair-cells, 
there expanding into a thickened 
extremity, known as the pharyn¬ 
geal process. These processes of 
Deiters’s cells with their terminal 
enlargements, or phalanges, enter 
into the formation of a reticulum 
surrounding the hair-cells and presenting spaces above through which 
the hair-processes project. External to the hair-cells and supporting 
cells of Deiters are several rows of elongated cells which form the 
outer edge of Corti’s organ. They are known as Hensen’s cells (H. C.). 
External to this, the basilar membrane is covered by a single row 
of cubical cells, called the cells of Claudius (Cl. C.). 

The membrana tectoria (Fig. 158, M.T.) is a peculiar structure described 
by Schafer as being composed of “fine fibrils embedded in a gelatinous 
matrix.” It is attached by a thin edge to the limbus external to the origin 


Fig. 158. —Organ of Corti (after Schafer). 
R, Membrane of Reissner; L, limbus; N, cochlear 
nerve; Lam.sp., lamina spiralis; I.H.C., inner hair- 
cells; O.H.C., outer hair-cells; I.R.C., inner rod 
of Corti; O.R.C., outer rod of Corti; T.C., tunnel 
of Corti; M.sp., membrana spiralis; D.C., cells of 
Deiters; H.C ., Hensen’s cells; Cl.c., cells of Claudius; 
Lig. sp., ligamentum spirale. 



Fig. 159.—Inner (a) and outer (b) rods of Corti 
(after Retzius). 
























272 


ANATOMY AND PHYSIOLOGY OF LABYRINTH 


of Reissner’s membrane. From this point it extends outward over the 
organ of Corti. From its attachment to the limbus to its outer ex¬ 
tremity, it increases greatly in thickness. Its upper surface is somewhat 
convex; its under surface— i.e., that apposed to, or covering, Corti ’s organ 
*—is irregularly concave. Owing to its varying appearances in different 
preparations, its dimensions are variously described by different authors. 
Thus Schafer states that it extends externally only over the region of the 
outer hair-cells, while A. A. Gray states that it extends outward as far as 
the extreme outer limit of the organ of Corti. As seen in microscopic sec¬ 
tions a very considerable space usually intervenes between the free surface 
of Corti’s organ and the superimposed tectorial membrane. Apparently 
most observers believe, however, that the normal relation of the two 
structures during life is one of actual contact (Schafer, A. A. Gray 
Shambaugh). 

The Cochlear Nerve .—The cochlear branches of the auditory nerve 
enter the cochlea by numerous minute perforations in the circular depres¬ 
sion at the base of the modiolus (fossa cochlearis, Fig. 145, a). This depres¬ 
sion is situated in the anterior wall of the internal auditory meatus, near 
its fundus, and below the opening of the facial canal from which it is sep¬ 
arated by a prominent ridge. It presents a central orifice leading into the 
central canal of the modiolus, around which are ranged the minute per¬ 
forations, or foramina (tractus spiralis foraminosus), through which pass 
the branches supplying the first two turns of the cochlea. The nerve- 
fibres entering this tract pass directly to the base of the spiral lamina. 
At the base of the spiral lamina as it winds around the modiolus is a spiral 
space in which are collected ganglion-cells, forming the spiral ganglion of 
the cochlea (Fig. 157, k). From the cells of this ganglion nerve-fibres 
radiate outward in the channels between the plates of the spiral lamina, 
perforating its outer plate to reach the basilar membrane and organ 
of Corti. On entering the neuro-epithelium of Corti’s organ, the nerve- 
filaments lose, their medullary sheaths, their axis-cylinders then passing 
between, and in contact with, the supporting cells of Deiters, the rods of 
Corti, and the hair-cells. They have not, however, been traced directly 
into the hair-ceils, and their exact terminal distribution is not yet known. 

The nerve-fibres passing through the central canal of the modiolus 
are distributed to the last half-turn of the cochlea. 

I estibular Nerve. The distribution of the peripheral branches of the 
vestibular nerve has already been described in connection with the cristse 
acusticae and macuke acusticae of the vestibular apparatus. In the in¬ 
ternal auditory meatus the vestibular portion of the auditory nerve is 
divided into two branches, i.e., an upper branch which supplies the 
utiicle and ampullae of the horizontal and anterior vertical canals, and a 

lower branch which supplies the saccule and ampulla of the posterior 
vertical canal. 

Central Fibres. Within the internal auditory meatus the cochlear and 
vestibular branches are traced to their common trunk, which passes in- 


THE BLOOD-VESSELS OF THE LABYRINTH 


273 




ward across the subarachnoid space toward the restiform body. Accord¬ 
ing to Dana, the nerve enters the medulla by two roots,—viz., a lateral or 
posterior root, composed chiefly of auditory, or acoustic, fibres, and a 
median or anterior root, made up chiefly of vestibular fibres. These roots 
communicate with three nuclei,—(1) the central nucleus (acoustic tubercle), 
situated on the floor of the fourth ventricle; (2) the ventral or accessory 
nucleus, which springs from the lateral root and lies between it and the 
median root; and (3) the large-celled nucleus (Deiters’s nucleus), which 
lies external to and below the central nucleus. The lateral root (auditory) 
communicates chiefly with the accessory nucleus, but is connected also 
with the other nuclei. From the central and accessory nuclei auditory 
fibres are sent to the temporal lobes of both hemispheres, but more fibres 
go to the opposite than to the corresponding side of the brain. The cor¬ 
tical centre for hearing is located in the first and second convolutions of 
the temporal lobe; and, since the basal nuclei of either ear send more 
auditory fibres to the opposite side of the brain than its own, it is clear 
that destruction of the cortical centre on one side will result in impairment 
of function which will be more pronounced in the ear opposite to the 
cortical lesion. 

The median root of the auditory nerve, composed chiefly of vestibular 
fibres, is principally connected with Deiters’s nucleus and, through fibres 
leading from Deiters’s nucleus, with the cerebellum. 

The Blood-vessels .—The arteries supplying the labyrinth are derived 
from one vessel,—the internal auditory artery, a branch of the basilar 
artery. This vessel breaks up within the internal auditory meatus into 
branches which in a general way follow the course of the branches of 
the auditory nerve. To the vestibule it supplies three branches,—one to 
the utricle and the horizontal and anterior vertical canals, another to the 
posterior vertical canal, and a third to the saccule. The cochlear division, 
before entering the spaces in the spiral lamina, breaks up into a network 
of anastomotic loops, from which small terminal vessels are sent to supply 
small circumscribed areas of the basilar membrane, organ of Corti, and 
outer wall of the cochlear duct (Shambaugh). According to Siebenmann, 
the venous blood is returned mainly along three channels,—viz., veins 
leading from the cochlea into the internal auditory meatus, and veins 
leaving the labyrinth by the aquaeductus vestibuli and aquaeductus cochleae 
respectively. Shambaugh, 1 who made careful studies of the blood-vessels 
of the labyrinth in the pig, sheep, and calf, found in these animals but one 
venous channel, which left the labyrinth along the aquaeductus cochleae 
and apparently drained the entire labyrinth. He refers to the work of 
Eichler upon the blood-vessels of the human ear, who “found but two 
routes by which the venous blood left the labyrinth, the vein of the aquae¬ 
ductus cochleae and the vein of the aquaeductus vestibuli.” Eichler’s 
conclusions have received the support of Politzer._ 

1 Shambaugh: Some Relations of the Blood Supply of the Inner Ear, Arch, of 
Otol., vol. xxxv, No. 1, 1900. 

18 







274 


ANATOMY AND PHYSIOLOGY OF LABYRINTH 


Physiology of Sound Perception (Cochlear Function). —In 
attempting to place before the reader a brief synopsis of this rather difficult 
subject, it may be well to acknowledge that the modern conception of 
the physiology of sound perception is based largely upon hypothesis 
and only to a limited extent upon demonstrable facts. There are, however, 
a few basic facts relating to the cochlear function, acceptance of which 
may now be assumed. We know, for example, that the cochlea is supplied 
by the cochlear branch of the auditory nerve, and that, when this cochlear 
nerve is completely destroyed or divided, total deafness of the correspond¬ 
ing ear results. We know also that destruction of the cochlea, either by 
disease or by surgical removal, invariably gives rise to total deafness. Of 
this there can be no shadow of doubt. The occasional xeports of cases in 
which there has been apparent retention of hearing after surgical removal 
of the cochlea are unquestionably to be explained by the failure of the 
observer to exclude the compensatory function of the sound ear. 

Since, therefore, we may produce deafness by destroying either the 
cochlea itself or the cochlear nerve before it enters the cochlear fossa at 
the base of the modiolus, and since the branches of the cochlear nerve 
have been traced to the basilar membrane and organ of Corti, we may 
confidently assume that the basilar membrane and organ of Corti are 
structures which are essential to the function of tone perception. So far 
we are dealing with indisputable fact. Attempting to go beyond this, we 
come quickly upon Helmholtz’s theory of tone analysis, a hypothesis 
which has formed the basis of most subsequent investigations which have 
yielded practical results. 

Up to the time of Helmholtz’s investigations, the study of the physi¬ 
ology of the cochlea had been obscured by certain mistaken views as to 
the anatomy of the labyrinth. In the seventeenth and eighteenth cen¬ 
turies it was generally believed that the labyrinth spaces contained air 
instead of fluid; and later the conception of the cochlear function was 
distorted by the belief that the fibres of the basilar membrane were longest 
at the cochlear base and diminished gradually as the apex was approached. 
W e now know that exactly the reverse is true. 

Helmholtz's theory is to the effect that the perception of musical tones 
is brought about by vibration o'f the basilar membrane in response to sound 
waves from without, and that the analysis of musical sound into tones of 
different pitch is explained by the hypothesis that different parts of the 
basilar membrane vibrate in response to sound waves of different pitch. 
In other words, that a soundwave consisting of a certain number of rhythmic 
double vibrations per second can induce movements only in certain fibres 
of the basilar membrane, other fibres being stimulated only when the 
number of rhythmic vibrations is either increased or diminished. And 
since the radiating fibres of the basilar membrane— i.e., stretching from 
the outer edge of the spiral lamina to the spiral ligament—are longest at 
the apex of the cochlear pyramid and shortest at the tympanic-vestibular 
end, it is assumed that the highest tones of the musical scale are produced 


WITTMAACK’S EXPERIMENTS 


275 


by movements of that portion of the basilar membrane nearest the vestibu¬ 
lar and round windows, and that the lowest tones correspond to vibrations 
of portions of the membrane nearest the apex or helicotrema. 

The Helmoltz theory is the theory of sympathetic vibration; i.e., it 
proclaims that only certain parts, or certain fibres of the basilar membrane 
can respond to, or vibrate in response to, an serial stimulus, or vibration, of 
given pitch, or vibration rate. At best it is a hypothesis, but a hypothesis 
which threw enormous light upon the significance of the structurally com¬ 
plex mechanism of the organ of Corti. The objections to it have been 
chiefly upon physical grounds; e.g., the unsuitable conditions for vibration, 
as we understand it, inherent in, and surrounding, the radiating fibres of 
the basilar membrane. This, it seems to the writer, is in accordance with a 
naive and common human propensity, which insists upon literal translation 
of terms, and accepts with difficulty any thesis which cannot be explained 
by analogy with commonly known facts and phenomena. Admittedly the 
radiating fibres of the basilar membrane are not analogous to the strings 
of a piano in their mode of sympathetic response to sonorous stimuli 
from without. 

That certain definite areas of the basilar membrane and organ of Corti 
have to do with the perception of certain tones has been supported by the 
studies of Wittmaack. 2 Wittmaack’s experiments consisted in subjecting 
animals during prolonged periods to hearing constantly a certain note,— 
e.g., 256 d.v., 1024 d.v., etc.,—the animals later being killed and the coch¬ 
lear structures examined under the microscope. It was found that certain 
definite areas of Corti’s organ, corresponding constantly to certain tones, 
gave evidence of pathologic change as a result of the prolonged stimulation 
or strain; and, further, that high tones produced morbid changes near the 
vestibular end of the scala media, and that low tones gave rise to changes 
nearer the helicotrema. These results have been confirmed by the investi¬ 
gations of Siebenmann. 

A belief which has become part of the accepted hypothesis is to the 
effect that some interaction between the organ of Corti and the membrana 
tectoria is essential to the proper transmission of auditory impressions to 
the brain,—or, to be more explicit, that friction or impact of the project¬ 
ing hair-processes of the hair-cells covering the organ of Corti against the 
under surface of the tectorial membrane is in some way essential to the 
function of tone perception. As to the method, or process, by which this 
contact or friction is brought about, the consensus of opinion among 
physiologists has strongly supported the view that sound waves, propagated 
through the perilymph and reaching the under surface of the basilar mem¬ 
brane, have there caused vibration or displacement of certain of its fibres 
thus carrying the corresponding hair-processes of Corti’s organ against the 
tectorial membrane. 

Naturally many theories and modifications of theories of sound per- 

2 Wittmaack: Ueber Schaedigung des Gehor durch Schalleinwirtung, Zeitsch. f. 
Ohrenheil., Bd. 50, 1908. 




276 


ANATOMY AND PHYSIOLOGY OF LABYRINTH 


ception have from time to time been advanced which, though exceedingly 
interesting, cannot be brought within the limited space of this handbook. 

The theory of Sir Thomas Wrightson and Sir Arthur Keith is based 
upon an intensive study of wave forms and elaborate experiments to deter¬ 
mine the direction of fluid sound waves within the cochlea and to explain 
mechanically the influence thereby exerted upon the essential structures 
of the organ of Corti. It is assumed that each inward movement of the 
stapedial foot plate imparts to the cochlear fluids an impulse which is 
immediately transmitted throughout their entire mass. According to this 
theory, the fluid sound wave travels, not by way of the scala vestubuli and 
through the helicotrema to the scala tympani, but passes directly through 
Reissner’s membrana and the scala media to the scala tympani, this mass 
movement being, of course, compensated for by an outward movement of 
the membrane of the round window. With these mass movements of the 
cochlear fluids the basilar membrane and the organ of Corti are depressed 
inward toward the scala tympani. The interaction of the hair-cells of 
Corti’s organ and the membrana tectoria are brought about by the to and 
fro movements of the basilar membrane. An effort is made to bring the 
movements of the hairs of the hair-cells into relation with what Wrightson 
calls the four phases of a simple sound wave, or rather the four phases of a 
single double vibration. 

Wrightson’s theory apparently relegates Reissner’s membrane and in 
fact the scala media to a status of complete functional insignificance. 
Though ingenious and interesting, it is, in the author’s opinion, unconvincing. 

The theories of Siebenmann and Shambaugh, giving a major function 
in vibration to the membrana tectoria, have found comparatively few 
followers, one obstacle to their acceptance being the apparently inherent 
unfitness of this structure to assume this role. 

Of modifications of the Helmholtz theory, the most satisfying, in the 
author’s opinion, is that of Dr. Albert A. Gray of Glasgow. According to 
this theory, the basilar membrane may vibrate in response to a sound wave 
over a considerable area; but there is a point of maximum amplitude of 
vibration, varying with the pitch or vibration rate. In other words, while 
the vibration may involve considerable portions of the basilar membrane, 
the point of maximum amplitude varies with each change of pitch, or vibra¬ 
tion rate; and it is the note corresponding to this point of maximum vibra¬ 
tion which is recorded in the cerebral hearing centre, and therefore appre¬ 
ciated as a musical tone. This theory is the more satisfying for the reason 
that, while robbing the Helmholtz theory of none of its essential features, 
it removes one of the chief obstacles to its acceptance, i.e., the conception 
of vibrations propagated through the cochlear perilymph which would not 

3 Siebenmann: Bardelben’s Handb. d. Anat. d. Menschen. 1897. 

4 Shambaugh: Physiology of the Cochlea, Annals of Otol., Sept., 1910; Physiology of 
Tone Perception, Dec., 1910. 

5 Gray: Various Theories of Hearing; Journal of Laryngol. and Otol., p. 391. 




PHYSIOLOGY OF THE VESTIBULAR APPARATUS 277 


induce movements in the basilar membrane more extensive than are 
allowed for in the Helmholtz hypothesis. 

The Vestibular Apparatus. —-The membranous vestibular apparatus 
consists of the utricle, saccule, and three semicircular canals. Whatever 
may be their exact function in health, it is probable that these structures 
act in concert. Injury to any one canal causes subjective and objective 
phenomena very similar to those following injury of the other two, or to 
the parts resting within the bony vestibule. The phenomena of vestibular 
irritation have been carefully studied both experimentally and clinically 
by Flourens, Goltz, Breuer, Crum-Brown, Ewald, Barany, Neumann, 
Ruttin, Hinsberg, Jansen, and a host of observers in different parts of the 
world. These observations, while of immense value in their bearing upon 
the symptoms of acute tympanic disease, have thrown but little direct 
light upon the vestibular function in health. They will not, therefore, be 
considered in the present chapter. 

We know that the vestibular mechanism is not an organ essential to 
man’s power of equilibration, for after its complete removal the individual’s 
equilibrium is soon re-established. By a somewhat similar course of logic 
the theory of Ewald— i.e., that the vestibular apparatus is in some degree 
responsible for the tone of the skeletal muscles—must be discarded, for 
destruction of the canals does not seem to influence muscular tone inju¬ 
riously. The author has had the opportunity of examining two individuals, 
a man and a woman, in whom the function of both labyrinths was absolutely 
and apparently permanently ablated, and these patients seemed to be 
rather above the average in muscular strength and potential efficiency. 

It is probable that the vestibular mechanisms are in one sense organs of 
orientation, in that they enable man under all conditions,— i.e., in light or 
darkness, and in whatever position his body may be placed,—subcon¬ 
sciously and without effort to determine the position of the different parts 
of his body. It is the sudden withdrawal of this power which places the 
individual after removal of one or both labyrinths, and even after he has 
recovered from the first vestibular disturbances incident to the operation, 
in some danger of serious accident. That he soon learns to guard against 
such mishaps under all or any conditions does not disprove the value of 
these organs in health. It proves simply that certain other faculties—- 
e.g., the so-called muscle, arthrodial, and tactile senses and the sense of 
sight—-have so enlarged their scope as to compensate for that which he has 
lost. Viewed in this way, it would seem that, if we permitted outselves 
to speak of the cochlear branch of the auditory nerve as the auditory 
branch, we might with equal propriety regard the vestibular branch as 
the nerve of orientation. 

The Otolith Apparatus.— In recent years there have been recorded 
several observations of a peculiar form of nystagmus, somewhat resembling, 
vet clearly distinguishable from, that induced by rotation. Baian\ 

6 Barany: Disease of the Otolith Apparatus; Journal of Laryng. and Otol., vol. 
XXXVI, p. 229. 




278 


ANATOMY AND PHYSIOLOGY OF LABYRINTH 


recorded the case of a man suffering from multiple sclerosis who, if the head 
was inclined toward the right shoulder, no matter how slowly, regularly 
exhibited a marked horizontal nystagmus to the left. That it was not due 
to displacement of endolymph in the semi-circular canals, but rather to the 
effect of position, was proved by the very gradual changes of position which 
caused it and also by its long persistence, i.e., provided that the inclined 
position of the head was maintained. This phenomenon is believed to be 
brought about through a disturbance of the so-called otolith apparatus or, 
to be more exact, of the saccule and utricle, though the exact nature of the 
imbalance by which it is produced has not been determined. 

During the past few years, much experimental work has been done, 
chiefly in the University of Utrecht and under the direction of Professor 
Magnus and Dr. deKleijn, to determine more definitely the exact function 
of the Saccule and Utricle. While these experiments are interesting, their 
practical bearing upon health and disease has not yet been sufficiently 
established to call for their inclusion in a handbook on otology. Students 
who wish to follow these investigations in detail will find in the short and 
interesting monograph of Dr. Alex. H. Tweedie 7 of Nottingham, England, 
a brief outline of this work, to which has been appended a rather compre¬ 
hensive bibliography. 

Whatever the exact function of the vestibular mechanism may be, it is 
fairly certain that the essential structures are the cristse acusticse of the 
semicircular canals and maculae acusticae of the saccule and utricle. Both 
histologically and physiologically there appears to be a certain analogy 
between these structures and CortPs organ. Thus, both the organ of 
Corti and the cristae and maculae acusticae are covered by a highly-organ¬ 
ized neuro-epithelium, of which the surface strata are composed of hair- 
cells from which hair-processes project. In each of these organs the hair- 
pi ocesscs pioject into, 01 toward, an important superimposed structure, 
friction or impact against which is essential to its proper performance of 
function. Thus the hair-cells of the cristae acusticae do not project directly 
into the endolymph of the ampullae, but into the soft cupola terminalis 
covering them. The hair-cells of the maculae acusticae are in contact with 
the otolith-holding membrane, while the hair-cells of Corti’s organ project 
toward the under surface of the membrana tectoria. According to Sham- 
baugh, the relation of the free surface of the organ of Corti and the tectorial 
membrane is one of actual contact. In the organ of Corti, impact of the 
hair-processes against the membrana tectoria is brought about through 
the agency of sound waves propagated through the labyrinthine fluids. 
In the case of the cristse acousticse and maculse acusticse, interaction is 
brought about between their hair-processes and the cupola terminalis and 
the otolith membrane by sudden changes in the position of the head The 
importance of this structural and physiological analogy between the different 
paits of the membranous labyrinth has been emphasized by Shambaugh. 

1922 7 r n W 213 ie: Utncular and A11 kd Reflexes; Journal of Laryn. and Otol., 




CHAPTER XI. 


INFLAMMATORY AND SUPPURATIVE LESIONS 
OF THE LABYRINTH. 

Suppurative labyrinthitis is unquestionably one of the most dan¬ 
gerous lesions with which the physician has to contend. The disease is 
practically always secondary to purulent disease of the middle ear or 
mastoid. The initial symptoms— i.e., those which announce the actual 
invasion of the membranous labyrinth—are invariably such as may be 
attributed to vestibular irritation. Unfortunately, universal familiarity 
with the phenomena of vestibular irritation can not as yet be assumed. 
It may be well, therefore, before discussing the clinical aspects of the 
disease, to review briefly certain experiments, facts, and accepted theories 
upon which our present knowledge of suppurative labyrinthitis depends. 

The experiments of Flourens 1 upon pigeons and rabbits, published in 
1824, established the fact that section of any one of the semicircular canals 
gives rise to uncontrollable movements of the head and eyes in the plane of 
the canal experimented upon. Breuer in 1888 demonstrated that similar 
phenomena could be induced by simple irritation of a canal without caus¬ 
ing its actual destruction,— e.g., by electrical, thermal, or chemical irritants. 

In 1892, Professor Ewald, of Strasburg, carried these experiments 
further, corroborating the results of Flourens, Breuer, and others, and 
establishing further the relation 
between endolymph movements 
in the different canals and the 
character and direction of the 
resulting nystagmus. These latter 
experiments are so clearly the 
basis of our present knowledge 
of the phenomena of vestibular 
irritation that we shall take time 
to describe them briefly. 

Ewald’s Experiments (Fig. 

160)—Ewald 2 experimented upon 
pigeons in the following way: 

Having exposed the canal selected 
for investigation, a small hole 

was drilled into it near its small end, and the lumen of the canal 
was obliterated at this point by the introduction of a lead mass. 
A second opening was next made between the small occluded end and 

1 Flourens: Les proprietes et les fonct.ions du systeme nerveux, pp. 454-482. 

2 Ewald: Physiologische Untersuchengen liber das Endorgon des Nervus Octavus, 

pp. 255-266. 

1 279 



Fig. 160.—Semicircular canals of pigeon (after 
Ewald). 





280 


LESIONS OF THE LABYRINTH 


the large, or ampullar, end of the canal. Into this second opening was 
introduced and fixed one end of a small hollow cylinder, open at both 
ends, the outer end of which communicated by means of a piece of narrow 
rubber tubing with a compressible rubber ball or bulb. The interior of 
bulb, tubing, and cylinder being now directly continuous with the lumen 
of the canal, it is clear that compression of the bulb must necessarily cause 
displacement of the endolymph in the membranous canal involved; and, 
since the small end of the canal has been obliterated, it is obvious that 
during compression, the endolymph movement must be toward and through 
the ampulla and into the cavity of the utricle. Beginning with a partially 
compressed bulb, it is equally clear that release of pressure will cause a 
movement of endolymph from the utricle toward and through the ampulla 
and in the direction of the small end of the canal. 

Ewald by this method experimented separately on the three semi¬ 
circular canals, and obtained the following results: 

Right Horizontal Canal. —Compression of the bulb (causing endolymph 
displacement toward the ampulla) was invariably followed by a slow strong 
movement of the head, exactly in the plane of the canal, toward the left. 
Coincidently with this head movement, the eyes were moved, also in the 
plane of the canal, to the left. On release of pressure the head and eyes 
quickly returned to their normal position. Suction (causing endolymph 
movement from the utricle through the ampulla and toward the small 
end of the canal) was followed by slow turning of the head and eyes, 
always in the plane of the canal, to the right. 

This experiment upon the left horizontal canal gives rise to similar 
movements of the head and eyes, but in reversed directions. 

Right Posterior Vertical Canal. —Compression (i.e., endolymph displace¬ 
ment toward and through ampulla) is followed by gradual movement 
of the head and eyes exactly in the plane of this canal and in the direction 
of its ampulla,— i.e., to the right. Suction gave rise to movements in the 
same plane, but in the opposite direction,— i.e., to the left. 

The reactions of the anterior vertical canal are similar to those of the 
posterior vertical, varying only in accordance with its different plane. 

Ewald’s experiments established definitely the following important 
facts: (1) Excitation of any single canal can produce nystagmus only in 
a plane parallel with the plane of that canal; (2) the relation between 
the direction of the endolymph movement in any canal and the direction 
of the resulting nystagmus is definite and constant; and, consequently, 
(3) by reversal of the endolymph movement in any canal we can reverse 
the direction of the induced nystagmus. 

The analogy between these experimental phenomena in the lower 
animals and vestibular nystagmus in man is now clearly established. As 
we shall see later, vestibular nystagmus in man is characterized by a quick 
movement in one direction and a slow movement in the opposite direction. 
With pigeons both head and eyes move in response to vestibular irritation, 
whereas in man the nystagmic movements are confined to the eyes. With 


CALORIC REACTIONS 


281 


regard to Ewald’s experiments, it is important that we bear in mind the 
fact that the slow movements of head and eyes caused by either compression 
or suction correspond to the slow component of a vestibular nystagmus. 
We are accustomed to name the direction of a vestibular nystagmus in 
accordance with the direction of the quick eye movement,— e.g., nystag¬ 
mus to the right, or nystagmus to the left. The quick eye movement does 
not, however, represent the vestibular impulse, which is responsible only 
for the slow eye movement in the opposite direction, the quick recoil 
movement being under the control of the central nervous system. 

Note. —The differentiation of the vestibular from the cerebral component of a 
vestibular nystagmus has been beautifully demonstrated in certain cases in which the 
caloric experiment—next to be described—has been employed upon a patient under deep 
anaesthesia. Narcosis having been pushed to the point where the peripheral reflexes are 
abolished, the caloric test has been applied in the manner usually giving rise to a ves¬ 
tibular nystagmus toward the opposite ear,—let us say to the left. Under these condi¬ 
tions, the vestibular activity being retained and the central nervous control having been 
suspended, the eyes, instead of executing successive quick movements to the left, are 
slowly rotated to the right and remain in that position. As the influence of the anaes¬ 
thetic wears off and the central reflexes are restored, the eyes are suddenly jerked from 
their position of deviation to the right, and execute the characteristic quick movements 
to the left. Or, if the narcosis is prolonged, the influence of the vestibular impulse may 
wear itself out, and the eyes return to their normal position. 

Barany’s Experiments; the Caloric Reactions. —It has long been 
known to otologists that irrigation of the ears for the removal of pus or 
cerumen will in some cases give rise to nystagmus, vertigo, and disturbance 
of equilibrium. This remained an unsystematized fact of no practical value 
in otology until the discovery by Barany, of Upsala, that these phenomena 
were not haphazard occurrences, depending upon individual idiosyncrasy, 
but were constant reactions having a definite relation to the temperature 
of the water used. 

The caloric reaction may be briefly stated as follows: If we irrigate 
either ear of a person with normal labyrinths with water of body tempera¬ 
ture, no subjective or objective symptoms are experienced. If we use 
water considerably below blood heat,— i.e., 86° F., or lower,—we invariably 
obtain the following reactions,—viz.: (a) rotary nystagmus of which the 
quick movement is in the direction away from the ear irrigated; (b) the 
patient experiences subjective vertigo, and (c) exhibits marked disturb¬ 
ances of equilibrium. Substituting hot water, i.e., at 110 F., we obtain 
exactly the same phenomena with the exception that the direction of the 
nystagmus is now toward the ear irrigated, and the ataxia shows certain 
changes in accordance with laws governing its relation to the nystagmus 
present. 

These reactions are very nearly invariable with normal persons. Their 
diagnostic value depends upon the fact that when the static labyrinth 
(vestibular apparatus) has been destroyed, either surgically or by disease, 
the vestibular nerve can no longer respond to stimulation by heat cr cold, 
and the caloric reactions are absent. 


282 


LESIONS OF THE LABYRINTH 


Note. —Barany’s explanation of these phenomena in accordance with Ewald s 
experiments is interesting and on the whole convincing. We must regard the whole 
labyrinthine cavity as an irregularly shaped vessel containing fluid (perilymph, 
endolymph), the temperature of which is presumably that of the blood. If, now, 
we bring hot or cold water in contact with one wall of this vessel, the temperature 
of that part of the contained fluid nearest this wall will be. raised or lowered. In 
other words, its specific gravity here will be increased or diminished, and it will sink 
or rise according to the physical laws governing fluids of different specific w r eight. 
Now, the parts of the semicircular canal system nearest the surface of the inner 
tympanic wall are the anterior half of the horizontal canal and the anterior or outer 

third and ampulla of the anterior vertical 
canal (Fig. 161). These parts are, there¬ 
fore, first influenced by the hot or cold 
water used in irrigating the ear. With 
the head erect, sudden cooling of the 
endolymph in the external (horizontal) 
semicircular canal does not give rise to 
an endolymph movement, this being pre¬ 
vented by its horizontal position. In 
the case of the anterior vertical canal, 
on the other hand, the part nearest the 
tympanum—viz., the outer or ampullar 
end—points directly downward. Irriga¬ 
tion with cold water would, therefore, 
in this canal give rise to a downward 
movement of endolymph toward and 
through its ampulla. That cold irrigation 
in normal individuals is always followed 
by rotary nystagmus toward the opposite 
side is in exact accordance with Ewald’s 
experiments. Further corroboration of 
this theory is obtained from the fact 
that if, immediately after irrigation with 
cold water, the head is bent downward 
so that the top of the head is directly 
toward the floor,—a position in which 
the endolymph movement would be re¬ 
versed,—the direction of the nystagmus is also reversed,— i.e., is toward the ear irri¬ 
gated. Further, if the head, after irrigation with cold, is quickly bent forward to 
an angle of 90 degrees so that the face looks directly downward, the nystagmus is 
changed from the rotary to the horizontal type. The explanation of this is not far 
to seek, for in this position of the head the anterior vertical and posterior vertical 
canals assume positions somewhere between the vertical and horizontal planes, while 
the horizontal canals fall quite in the vertical plane. The chief endolymph move¬ 
ment is therefore in the horizontal canal, with resulting horizontal nystagmus. That 
the use of hot water, which would reduce endolymph specific gravity, should give rise 
to nystagmus in reverse directions tends further to support Barany’s theory as to the 
causation of these interesting phenomena. 

Vestibular Nystagmus. —Involuntary eye movements occur as an 
exceptional phenomenon with several conditions having no relation to 
disease of the labyrinth, e.g., cerebellar lesions, certain ocular diseases, 
hereditary syphilis, neurasthenia. It is necessary, therefore, that a word 
be said as to certain characteristic features which distinguish vestibular 
nystagmus from other forms. To establish a claim to vestibular origin, 



Fig. 161.—Diagrammatic picture of inner tym¬ 
panic wall, showing (1) horizontal semicircular 
canal, and (2) anterior end of anterior vertical 
canal. 




VESTIBULAR NYSTAGMUS 


283 



Fig 162. 



Fig. 163. 



Fig. 164. 


(1) a nystagmus must be composed of a quick movement in one direction 
and a slow movement in the opposite direction; (2) it is increased, usually 
in rapidity and always in length of excursion, when the eyes are turned 
voluntarily in the direction of the quick movement; (3) it becomes weak, 
or may disappear wholly, when the eyes are turned 
in the direction of the slow nystagmic movement. 

The above are invariable characteristics of nystag¬ 
mus of vestibular origin, whether produced by experi¬ 
mental irritation or in the course of acute laby¬ 
rinthine disease. 

Vestibular nystagmus may be horizontal, oblique, 
vertical, or rotary. The nystagmus caused by acute 
labyrinthine disease is practically alwaj^s rotary. 

Obviously all forms of vestibular nystagmus are 
rotary, since in all the eye movements take the 
form of to-and-fro rotation about some imaginar}^ 
axis. The term “rotary,” however, is applied only to 
forms of nystagmus in which the eye movements as 
seen from in front do not seem to describe a straight 
line upon the cornea. We call all types of nystagmus 
“rotary,” therefore, in which our line of vision does 
not fall in the plane of the nystagmus. Thus, if our 
line of vision coincides with the axis of rotation,— i.e., 
is at right angles to the plane of rotation,—we have 
the most pronounced type of rotary nystagmus 
possible,—a veritable wheel nystagmus (Fig. 162). 

On the other hand, when our line of vision falls within 
the plane of rotation, there results a straight nystag¬ 
mus which may be horizontal (Fig. 163), vertical (Fig. 

164), or oblique (Fig. 165), but can not be rotary. 

When our line of vision falls somewhere between the 
axis of rotation and the plane of rotation, we have a 
form of nystagmus falling somewhere between the 
straight and the wheel type, and partaking somewhat of the character of 
each (Fig. 166). In such a nystagmus the excursion made by any given 
point upon the cornea will, as seen from in front, represent the arc of 
a circle much larger than one whose radius is measured by the distance 
between the centre of rotation and the corneal point in question. Such 
a nystagmus is also called “rotary,” and is the type usually seen in acute 
labyrinthine disease. 

From the results of Ewald’s experiments, and from a clinical study of 
nystagmus as seen in suppurative lesions of the labyrinth, we may deduce 
the following,—viz.: That, since irritation of a single canal can produce 
nystagmus only in its own plane, and since the nystagmus accompanying 
acute labyrinthine disease rarely corresponds exactly to the plane of any 
single canal, we may assume that suppurative invasion of the labyrinth 



Fig. 165. 



Fig. 166. 

Figs. 162-166.— Types of 
vestibular nystagmus. 




284 


LESIONS OF THE LABYRINTH 


almost invariably involves all, and always more than one, of the three 
semicircular canals. 

A little practice may be required to detect the rotary character of the 
nystagmus usually accompanying acute labyrinthine disease, lo the 
unpractised eye the ocular movements may at first seem quite in the hori¬ 
zontal plane. If, however, we fix our attention upon some dilated corneal 
vessel and note carefully its changing relation to the border of the lower lid, 
the rotary element becomes unmistakable. Lack of attention to this point 
has doubtless been responsible for some obviously incorrect clinical reports. 

Physiological Nystagmus.— This term has been applied by Barany 
to a form of nystagmus which is seen in many normal persons when the 
eyes are voluntarily placed in the extreme lateral position in either direction. 
It is mentioned in this place because it is of the greatest importance that 
the student should learn to recognize it as having no significance as an 
indication of suppurative labyrinthitis. The character of the eye move¬ 
ments is quite similar to that above described,—that is to say, it is usually 
rotary in character and is composed of a quick movement in one direction 
and a slow movement in the opposite direction. It is, however, easily 
differentiated from the nystagmus of labyrinthine disease by the following 
points: 

(a) Spontaneous vestibular nystagmus in its most active stage is 
constant, but is exaggerated when the eyes are voluntarily turned in the 
direction of the quick movement. Physiological nystagmus is present 
only when the eyes are turned strongly in one or the other lateral direction, 
and then usually lasts but a few seconds. 

(b) Vestibular nystagmus in its active stage is present whatever the 
position of the eyes. Later, however, as the strength of the nystagmus is 
gradually reduced, it may be wholly absent when the eyes are turned in 
the direction of the slow nystagmic movement. Physiological nystagmus 
changes its direction according to the position of the eyes,—the quick 
movement corresponding to the lateral direction in which the eyes are 
voluntarily turned. 

(c) Vestibular nystagmus in its most active stage is almost invariably 
accompanied by vertigo and ataxia, and these symptoms, even after the 
nystagmic movements have grown weaker, can usually be reinduced by 
sudden movements of the head. Physiological nystagmus is absolutely 
unaccompanied by any subjective symptoms. 

Barany’s estimate that this so-called physiological nystagmus occurs 
in 60 per cent, of normal persons seems to me exaggerated,—20 to 25 per 
cent, being, according to my observation, nearer the correct proportion. 

Rotation or Turning Experiment. —This is simply another method 
of inducing endolymph movements in the semicircular canals and thereby 
causing symptoms of vestibular irritation. 

When a normal person, seated, with head erect, upon a revolving 
chair (Fig. 167), is suddenly and forcibly rotated in one or other direction, 
•—let us say to the right,—there occurs a horizontal nystagmus with the 



Fig. 167.—Revolving chair: patient and physician in position for rotation test. 















THE SEMICIRCULAR CANALS 


285 


quick eye movement in the direction in which he is turned,— i.e., to the 
right. When the rotations are suddenly stopped, the direction of the 
nystagmus is reversed,— i.e., it is now to the left. The average duration of 
this so-called “after nystagmus” is about 40 seconds. 

The rotation experiment is a useful aid in the study of vestibular 
phenomena in that, by placing the head during rotation in various posi¬ 
tions, one is able to induce at will almost any form of vestibular nystagmus. 
Obviously the various forms of nystagmus, vertigo, and ataxia can mean 
little to the student who has not a correct mental picture of the planes of 
the three semicircular canals, and also of the relative positions of their 
ampullar and small ends. These relations seem often to present such 
difficulties to the beginner that the writer is tempted to suggest a very 
simple device by which, with the aid of two visiting cards, one may easily 
fix them in memory. 

In Fig. 168, a-b represents a line throughout which the card is to be 
cut or divided by a sharp-pointed knife; c-d, a line at which the card is to 
be bent or folded upon itself. If now we bend the card at c-d, so that the 



Fia. 168. Fia. 169 * 

Fias. 168 and 169.—Author’s scheme for remembering semicircular canal planes. 


two segments occupy planes at right angles to each other, and insert be¬ 
tween the cut edges, now also bent at right angles, the edge of a second 
card (Fig. 169), we have three planes, each at right angles to the other two. 

If we wish this little improvised model to represent the planes of the 
three canals of the right ear, we have only to hold it (mentally) to the side 
of the head, with the bisecting card in the horizontal plane, and its edge, 
d-e, parallel with the anteroposterior axis of the skull. In this position 
we have the upper half of the anterior segment of the vertical card (a) 
representing the plane and position of the anterior vertical canal, the 
middle part of the posterior segment ( b ) representing the posterior vertical 
canal, and the enclosed part of the inserted card ( c ) representing plane 

and position of the horizontal canal. 

If we wish this model to represent also the respective curves and the 

































































286 


LESIONS OF THE LABYRINTH 



Fig. 170. 


ampullar and small ends of the three canals, we must outline these struc¬ 
tures upon the cards as indicated in Figs. 170 and 171, and with scissors 

cut away part of the card (Fig. 

171), as indicated by the dotted 
lines. When these cards are cut, 
folded, and adjusted (Fig. 172), 
we have clearly before us the com¬ 
mon opening of the anterior and 
posterior vertical canals (a), the 
ampulla of the anterior vertical 
canal (6), the ampulla of the hori¬ 
zontal canal (c), and the ampulla 
of the posterior vertical canal (d). 

Explanation of Rotational Nys¬ 
tagmus .—When the head, held in 
the erect position, is suddenly 
turned in the horizontal plane 
either to the right or left, the 
endolymph in the two horizontal 
canals, by reason of its inertia, 
at first lags behind,— i.e., is dis¬ 
placed in the opposite direction. 
If, for example, the head is turned 
to the right, the initial endo¬ 
lymph movement will in the 
right horizontal canal be toward 
its ampulla, while in the left 
hoiizontal it will be toward the 
small end of the canal (see Fig. 
173). Now, according to Ewald’s 
experiments, these are precisely 
the endolymph movements which 
in these canals should produce 
nystagmus to the right, and this 
phenomenon is always present 
during the rotations to the right. 
When the rotations are suddenly 
stopped, the endolymph, this 
time by reason of its momentum, 
is displaced in the opposite direc¬ 
tion, with the result that the 
direction of the nystagmus is re¬ 
versed,— i.e., it is now to the left. 




Figs. 170, 171, and 172.—Author’s scheme for remem. 
bering exact relative positions of the three canals. 


Note. —When a normal individual is rotated about a vertical axis, the influence of 
the rotations upon any particular canal will depend upon the relation which the plane 
of this canal bears to the horizontal plane. If the canal in question lies quite in the 



















































SYMPTOM COMPLEX OF VESTIBULAR IRRITATION 287 


horizontal plane, the influence of rotation will reach its maximum, and will produce a 
maximum endolvmph displacement. As the plane of the canal departs from the hori¬ 
zontal, the influence of rotation in the horizontal plane is diminished, and becomes 
progressively less in exact proportion as the angle of extension between the plane of the 
canal and the horizontal plane is increased. Finally, when the canal assumes the ver¬ 
tical plane, no displacement of endolymph results from rotation about a vertical axis. 
It is obvious, therefore, that with head erect, rotation in the horizontal plane influences 
only the two horizontal canals, the an¬ 
terior and posterior vert ical canals being 
eliminated by their position. If, how¬ 
ever, the head during rotation is bent 
forward so that the face looks directly 
downward, the horizontal canals will 
be made to assume the vertical plane, 
while the posterior vertical canals will 
be brought more into the horizontal 
plane. Rotation with the head in this 
position will therefore be followed by 
rotary nystagmus. 



Fig. 173. — Diagrammatic picture of a horizontal 
section of skull, passing through horizontal semicircular 
canals, a. Large arrow indicating direction in which 
individual is rotated; b, small arrow = resulting en¬ 
dolymph displacement during rotation; c, medium 
arrow showing direction of quick eye movement dur¬ 
ing rotation. 


During rotation, then, we 
may, by changes in the position 
of the head, bring different canals 
under the influence of the experi¬ 
ment, and thus vary at will the 
form of nystagmus. In all cases, 
however, the direction of the nys¬ 
tagmus follows a definite rule, 
which may be briefly restated as 
follows: During rotation a person 
exhibits nystagmus in the direction 
in which he is turned. Arrest of 
rotation is immediately followed by 
nystagmus in the opposite direction. 

The diagnostic value of the 

rotation test and the method of applying it will be spoken of in con¬ 
nection with the latent stage of suppurative labyrinthitis. 

The Symptom Complex of Vestibular Irritation: Nystagmus, 
Vertigo, Ataxia. —Vestibular irritation, whether experimentally induced 
(e.g., by thermal, electrical, or mechanical stimuli) or resulting from acute 
labyrinthine disease, is almost invariably announced by three associated 
symptoms,—viz., spontaneous nystagmus, vertigo, and disturbance of 
equilibrium. These three phenomena are so constantly associated with 
the onset or acute stage of suppurative labyrinthitis that their absence 
during this period would of itself be sufficient to exclude the vestibule and 

static labyrinth as among the parts involved. 

Obviously, these symptoms, either singly or in association, may also 
be present in various conditions not dependent upon labyrinthine disease. 
Thus, nystagmus may occur with certain ocular lesions, with cerebellar 
abscess, with tumors occupying the posterior fossa of the skull, or ma} occur 










288 


LESIONS OF THE LABYRINTH 


as a physiological anomaly having no recognized pathological significance 
(“physiological nystagmus”). As with nystagmus, so may vertigo and 
ataxia result from many functional and organic disorders. It is very - 
important, therefore, that we be able to recognize certain distinguishing 
features, either in the symptoms themselves or in their relation to each 
other, as they occur in acute labyrinthine disease. 

In the first place, vestibular vertigo is always rotary in character,— 

i.e., is always accompanied by a subjective impression of the rotation of 
surrounding objects, and this subjective rotation is always in a plane cor¬ 
responding to the plane of the nystagmus. There can be no doubt that 
the very closest relation exists between vestibular vertigo and vestibular 
ataxia, and that the character of each depends upon the type of nystagmus 
present. Barany was the first to observe certain seemingly constant rela¬ 
tions between vestibular vertigo and ataxia and vestibular nystagmus, 
which he formulated somewhat as follows: 

1. Spontaneous vertigo of vestibular origin is always accompanied by 
some degree of spontaneous vestibular nystagmus, and is always increased 
when the eyes are voluntarily turned in the direction of the quick nystagmic 
movement. 

2. Vestibular ataxia is always accompanied by nystagmus, and is always 

influenced by the position of the head. 

3. A person exhibiting vestibular nystagmus tends to move within the 
plane of the nystagmus, and to fall in the direction opposite to the quick nys¬ 
tagmic movement. 

The writer believes that the above statements are in the main correct, 
and that what may seem to be occasional exceptions or contradictions will 
under more accurate methods of observation be recognized as apparent 
rather than real. The practical value of these hypotheses in furnishing us 
with criteria by which the value of single symptoms may be gauged must 
be apparent. Thus, vertigo which is not accompanied by nystagmus even 
when the eyes are turned strongly in one or other lateral direction, and 
ataxia which is not attended by nystagmus and is not influenced by changes 
in the position of the head, are certainly not suggestive of vestibular 
irritation. 

A word must also be said as to the reaction movement, or tendency 
which a person exhibiting vestibular nystagmus shows to fall in a certain 
direction. Barany’s law, it will be remembered, reads, “A person exhibit¬ 
ing vestibular nystagmus tends to move within the plane of the nystagmus, 
and to fall in the direction opposite to the quick nystagmic movement/’ 
It seems to me that we shall obtain a better understanding of the principle 
involved if we say that a person exhibiting vestibular nystagmus tends to 
rotate within the plane of the nystagmus and in the direction opposite to the 
quick eye movement. This tendency to rotation is about an axis passing 
through his head, and he falls, or tends to fall, in the direction in which 
this rotation throws his body, and this, as we shall see, is not always in 
the opposite direction to the quick nystagmic movements. 


/ 


ATAXIA OF VESTIBULAR IRRITATION 


289 


Let us take for example a person who has been turned rapidly in a re¬ 
volving chair ten times to the right, and who as a result exhibits well- 
marked horizontal nystagmus to the left. He now experiences pronounced 
rotary vertigo in which surrounding objects seem to rotate about him in 
the horizontal plane,—and usually to the left. Immediately after the 
rotations of the revolving chair are stopped, let him stand and, with head 
erect and feet approximated, close his eyes. The nystagmus being in the 
horizontal plane, the reaction movement should be, not falling, but grad¬ 
ual turning in the horizontal plane to the right (Fig. 174). This, however, 
may not be demonstrated, or may be shown only by a tendency to turn 
the head to the right. Let us now test Bar any \s proposition that vestibular 
ataxia is always influenced by the position of the head. Request him to 
incline the head forward to an angle of 90 degrees so that the face looks 
directly downward (Fig. 175). With this position of the head the 
plane of the nystagmus is changed from the horizontal to the vertical, and, 
the quick eye movement being to the left, the head tends to rotate to the 
right. This rotation of the head to the right results, however, in throwing 
his body in the opposite direction, and he falls to the left. In this case we 
seem at first glance to have a contradictory reaction, in that the subject 
falls in the direction of the quick eye movement. After a moment’s reflec¬ 
tion, however, and with Fig. 175 before us, it becomes clear that the rotation 
of the head in the direction opposite to that of the quick eye movement is 
precisely the factor which determines his falling to the left. If the head is 
inclined directly backward to an angle of 90 degrees so that the face looks 
directly upward, the rotation tendency will throw his body in the opposite 
direction,— i.e., he will fall to the right (Fig. 176). 

In acute suppurative labyrinthitis the nystagmus is of the same type 
as that induced by syringing the normal ear with cold water. The caloric 
test enables one, therefore, to investigate the ataxia accompanying the 
nystagmus seen in acute labyrinthine disease. Here, the nystagmus being 
rotary and falling therefore more nearly in the vertical plane, the patient, 
standing with head erect, tends to fall in the direction opposite to the 
quick eye movement (Fig. 177). In acute suppurative labyrinthitis, the 
nystagmus is practically always rotary and toward the sound ear, and hence 
the patient falls toward the diseased ear. 

Pointing Tests. —Closely related in origin or causation to the reaction 
movements (falling directions) are the phenomena brought out by the so- 
called pointing tests. The normal individual, with eyes closed and having 
located with a finger some fixed object by the sense of touch, can move his 
hand upward or downward in the horizontal plane and bring his finger 
again into contact with the object touched, or will miss it only by a 
fraction of an inch. This maybe called normal accuracy. In an individual, on 
the other hand, who exhibits the symptom-complex of vestibular irritation 
( e.g ., after rotation or the caloric test), pointing accuracy is lost, the hands in 
attempting without the aid of sight to move accurately in the vertical plane 
regularly diverging in the direction opposite to that of the nystagmus present. 
{For the theory and application of these important tests, see Chapter XIV.) 

19 



290 


LESIONS OF THE LABYRINTH 


From this short preliminary discussion of vestibular phenomena we 
must pass to a consideration of the lesions upon which they throw light. 
The subject of vestibular irritation is so many-sided and presents so many 
phases which are of practical or academic interest to the otologist, that it 
is no easy matter to condense one’s discussion into the narrow space limits 






Figs. 174, 175, 176 and 177.—Diagrams showing falling directions in relation to vestibular nystagmus. 
N arrow, direction of nystagmus; I)R arrow, direction of rotation or falling. 

of a manual of this character. Naturally, this is possible only by the elim¬ 
ination of much which one would like to include were more ample space at 
his command. 

The student who wishes to study for himself the variations in 
vertigo and ataxia in response to different forms of vestibular nj^stagmus, 
may do so by observing a person who has just been rotated upon a 












TYPES OF ROTATION NYSTAGMUS. 


291 


revolving chair. In order to facilitate such studies, we append below 
a synopsis of Barany’s 3 rules for determining in advance the form of 
nystagmus which shall follow rotation. 

“Sitting erect upon a revolving chair a person revolves about a vertical axis. If 
we now imagine his eye cut through in a horizontal plane,— i.e., by a plane at right 
angles to the axis about which he revolves,—it is evident that this section will describe a 
line upon the cornea which will vary according to the position of the head. This line 
will indicate the form of the nystagmus (Fig. 178). Thus, with head erect, the horizontal 
plane in bisecting the eye will form a line passing horizontally across the cornea, and 
produce a horizontal nystagmus (Fig. 178, A). With head bent laterally toward the 



Fig. 178. —Diagrams showing different forms of rotation nystagmus. 

shoulder so as to form an angle of 45° with the vertical, a horizontal section will be 
indicated by a line passing obliquely across the cornea, and produce an oblique nystag¬ 
mus (Fig. 178, B). If the head is bent fully toward the shoulder so as to form an angle 
of 90° with the vertical, the eye will be bisected in a plane at right angles to its trans¬ 
verse diameter, and give rise to a vertical nystagmus (Fig. 178, C). With the head 
bent forward so that the face looks directly downward, the horizontal plane would 
divide the orbit so as to remove a segment which would include the iris. It should, 
therefore, be indicated by a circular line about the iris. The character of the nystag¬ 
mus, however, is indicated by the points of contact at which the horizontal plane enters 
the orbit, and not by those at which it cuts its way out. With the head bent directly 
forward, therefore, a horizontal section is indicated by a curved line above the iris, and 
turning to the right will be followed by rotary nystagmus to the left (Fig. 178, D). 
With head bent directly backward so that the face looks upward, a horizontal section 
describes a curved line below the iris. With head in this position, rotation to the right 
is followed by rotary nystagmus to the left. But in this case the concavity of the nystag¬ 
mic curve is directed upward (Fig. 178, E).” 4 ___ 

3 Barany: Physiologie u. Pathologie des Bogengang-Apparates beim Menschen, 12-13. 

4 Kerrison: Phenomena of Vestibular Irritation, Annals of Otology, Rhinology, and 
Laryngology, Sept., 1909. 









292 


LESIONS OF THE LABYRINTH 


SUPPURATIVE LABYRINTHITIS. 

Under this head are grouped such lesions of the labyrinth as are sec¬ 
ondary to suppurative disease of the middle ear or mastoid. In the older 
of their importance and frequency, they may be mentioned as follows: 
Diffuse suppurative labyrinthitis, circumscribed suppurative labyrinthitis, 

diffuse serous labyrinthitis, perilabyrinthitis. 

Diffuse Suppurative Labyrinthitis. — Etiology. Suppurative laby¬ 
rinthitis is always secondary to a suppurative lesion originating elsewhere 
in the body,—usually within the middle-ear cavity. While it may be 
argued upon theoretic grounds that an infective process may reach the 
labyrinth by other pathways,— e.g., by the blood-vessels from a focus of 
infection within the tonsil or parotid gland, or by way of the vestibular or 
cochlear aqueducts from a suppurative lesion within the cranium, it is 
exceedingly doubtful if such modes of infection have been definitely estab¬ 
lished in any case in which tympanic suppuration was absent. 

For practical purposes, therefore, we may say that suppurative laby¬ 
rinthitis is always secondary to a suppurative process within the middle 
ear. The spread of an infection from the tympanum to the labyrinth may 
occur by any one of several routes, viz.: 

1. By erosion of the bone at some point upon the labyrinthine wall 
giving rise to a so-called labyrinthine fistula. The points at which such 
fistulse are seen may be mentioned in accordance with the frequency of 
their occurrence in the following order,—(a) horizontal semicircular canal, 
(b) oval window, involving necrosis of the stapedial foot-plate or mem¬ 
branes, and (c) some point upon the promontory. 

2. By extension of the inflammatory process through the bone, or by 
way of the minute anastomotic vessels without the production of a demon¬ 
strable fistula. 

3. Through invasion of the labyrinth from a deep-seated extra-dural 
abscess on the posterior surface of the petrous pyramid (Hinsberg). This 
pathway of infection is considered here because an extra-dural abscess at 
this point is usually of otitic origin. 

4. Infection of the labyrinth as a result of injury to the labyrinth wall 
during operation. Mygind 5 states that he has seen a considerable number 
of such cases, and records his belief that labyrinthine suppuration occurs 
more frequently as a result of traumatism incident to the radical operation 
than is generally recognized. That such a mode of infection must be con¬ 
sidered seriously is emphasized by the statement of Jansen 6 that in his 
own operative experience suppurative labyrinthitis has occurred in 16 
cases as a direct result of injuries inflicted during the radical operation, or 
subsequent curettage. Hinsberg 7 collected from the reports of other aural 
surgeons 25 cases of injury to the stapes during operation, two of which 

6 Mygind: Trans. Am. Med. Assoc., Otological Section, 1910, p. 189. 

6 Jansen: Trans. Am. Laryn., Rhin., and Otol. Society, 1908, p. 115. 

7 Hinsberg: Uber Labyrintheilerungen, p. 4. 




TYMPANIC SUPPURATION 


293 


ended fatally. To these he added a fatal case of his own. It is obviously 
incumbent upon us to give greater prominence to this possible source of 
infection than is accorded it in most text-books. 

Frequency of Labyrinthine Suppuration as a Complication of Suppurative 
Otitis Media. —This is a question almost impossible of exact solution. 
Undoubtedly many deaths have occurred as a result of intracranial com¬ 
plications in which an intermediate lesion of the labyrinth has been un¬ 
recognized and therefore ignored. Presumably the discrepancy in the 
percentages of cases developing suppurative labyrinthitis reported in 
different clinics has been due in part to the closer study, and therefore 
more exact knowledge, of the disease in certain clinics as compared with 
others. Thus, in Prof. Urbantschitsch’s clinic in Vienna, and in the Uni¬ 
versity-Polyclinic presided over by Prof. Hinsberg in Breslau, where the 
disease has been made the subject of special study, the number of cases- 
reported has been larger than elsewhere in Austria and Germany. 

According to Hinsberg, 8 one in every 100 cases of middle-ear suppura¬ 
tion develops suppurative labyrinthitis. Von Stein, 9 of Moscow, in 420 
cases of middle-ear suppuration operated on, found suppurative labyrin¬ 
thitis in 10 cases; he therefore places the percentage as high as 2.2 per cent. 
Hinsberg states his belief that infection of the labyrinth is a more frequent 
complication of tympanic suppuration than all the intracranial complica¬ 
tions (meningitis, brain abscess, sinus thrombosis) combined; and further 
that a very large percentage of all cases of meningitis and brain abscess 
following middle-ear disease are in reality secondary to an intermediate 
suppurative process involving the labyrinth. These statements are based 
partly upon his own observations and partly upon an analysis of the pub¬ 
lished reports of others. 

Of conditions within the middle ear rendering invasion of the labyrinth 
probable, all writers agree that the presence of cholesteatoma is the most 
potent factor. Jansen some years ago reported a series of 121 cases of 
suppurative labyrinthitis in which cholesteatoma was the apparent cause 
in 71 cases. Holinger, 10 after examining the literature bearing upon this 
question, concludes that a majority of cases of suppurative labyrinthitis 
are traceable to the influence of cholesteatoma. 

Tubercular lesions of the middle ear are also said to be responsible for 
many cases of labyrinthine disease (Siebenmann, Nager, Hinsberg). Aural 
tuberculosis, however, is more likely to cause widespread necrosis of the 
labvrinthine capsule without early signs of vestibular irritation. 

While either an acute or a chronic middle-ear suppuration may lead 
to labyrinthine infection, by far the greater number of cases are caused by 
the chronic form of suppurative otitis media. On the other hand, infec¬ 
tions of the labyrinth secondary to acute purulent otitis media seem to 
exhibit a greater tendency to spread rapidly to the meninges, and there- 

8 Hinsberg: ibid., p. 1. 

9 Von Stein: Annales des maladies de l’oreille, 1896, p. 30. 

10 Holinger: Trans. Section Laryng. and Otol., Ain. Med. Assoc., 1910, p. lo5. 









294 


LESIONS OF THE LABYRINTH 


fore to end fatally. This difference is presumably due in part to the greater 
average virulence of the acute tympanic infections. 

As to the comparative significance of different points of attack as in¬ 
fluencing the subsequent course of the disease, experienced observers "very 
generally agree that infection of the labyrinth through necrosis (fistula) of 
the external semicircular canal offers a much more favorable piognosis 
than do lesions in which the pathway of infection is through the oval or 
round window, or even through a necrotic defect in the promontory. As 
far back as 1907, Panse 11 emphasized his belief that fistula} of the semi¬ 
circular canals constitute a condition prognostically favorable so far as life 
is concerned. Somewhat in accord with this view is the statement of 
Hinsberg that in nearly all the fatal cases coming under his observation, 
one or both windows were perforated or “broken down” (“so ist in der 
Tat kein Zweifel dariiber moglich dass bei den todlich verlaufenden Fallen 
fast stets eins oder beide Fenster durehbrochen sind, wahrend Bogen- 
gangsfisteln bei ihnen sehr selter sind”). If these facts have any practical 
significance, they should teach us the danger of careless surgery in the 
neighborhood of the stapes and oval window. These are points which the 
student of practical otology will do well to think over and bear in mind. 

Symptoms. —As the labyrinth is composed of two distinct mechanisms, 
—viz., the cochlea and the static or vestibular apparatus ,—so the symptoms 
of diffuse labyrinthitis must fall under two heads,—(1) those due to impair¬ 
ment or loss of the cochlear function—(be., deafness), and (2) those due 
to disturbance of the static or vestibular function. 

Undoubtedly the most striking and characteristic phenomena of the 
disease are those referable to the disordered vestibule, and these will 
chiefly occupy our attention in the following pages. To appreciate properly 
these phenomena, it is necessary to recognize two distinct and clearly 
differentiated stages of vestibular disturbance,—viz., (a) an acute stage, 
characterized by symptoms of vestibular irritation: and (b) a latent or 
quiescent stage, characterized by vestibular paralysis. 

Clinical Features of the Onset and Acute Stage. —Since suppurative 
labyrinthitis is practically always secondary to purulent otitis media, 
there may be pre-existing symptoms referable to that disease, upon which 
those of the labyrinthine lesion are engrafted. 

The invasion of the labyrinth is usually announced by sudden and very 
distressing vertigo. If the patient has been previously confined to bed, as 
when the labyrinth is invaded during an attack of acute mastoiditis, the 
onset is less spectacular, and possibly somewhat less severe subjectively, 
than may be the case when the patient is up and about, under which cir¬ 
cumstances he may be overwhelmed by the suddenness and severity of the 
attack. If the patient does not fall, he usually requires support, and, as a 
rule, is obliged by the severity of the symptoms to go to bed. Following 
quickly upon the appearance of vertigo, nausea and vomiting frequently 


11 Panse: Arch, of Otol., Amer. edition, April, 1907, p. 87. 



SYMPTOMS: NYSTAGMUS, VEKTIGO, ATAXIA 


295 


add to the patient’s distress. Vomiting is often a persistent and frequently 
recurring disturbance during the first day or two of the attack. 

Nystagmus .—If the eyes are observed at this time, there will invariably 
be seen an active rotary nystagmus with the quick eye movements toward 
the sound ear. The eye movements are increased in rapidity and extent 
when the eyes are voluntarily turned in the direction of the quick nystagmic 
movement, and are noticeably diminished when they are turned in the 
opposite direction. The nystagmus is noticeable, however, and the direc¬ 
tion of the quick movement is unchanged, whatever the position of the eyes. 

The nystagmus accompanying suppurative labyrinthitis, while usually 
described as rotary, is really in most cases a combination of the horizontal 
and the wheel types (see Fig. 166 on page 282). 

Vertigo .—The vertigo also is of the rotary type, i.e., the patient has 
the impression that surrounding objects are rotating about him, sometimes 
in such bewildering fashion that he is unable to analyze and correctly de¬ 
scribe his sensations. When he is able to do so, it is found that the plane 
in which objects seem to rotate always corresponds to the plane of the 
nystagmus. When, therefore, he stands or is supported with head erect, 
objects seem to rotate about him in a plane approaching the vertical, but 
when he lies upon his back (i.e., with face turned upward), the plane of 
the nystagmus falls more into the horizontal plane, and his sensation is 
of the rotation of objects in the horizontal plane about him. 

The direction of seeming rotation varies; most usually it is from the 
side of the slow nystagmus movement. Thus, with head erect, objects 
seem to rise from the floor on the side corresponding to the diseased ear, 
and to fall or sink on the other side of his body. In some cases, however, 
the direction is reversed. If he closes his eyes, he has the sensation of 
himself rotating. If his eyes are voluntarily turned in the direction of the 
quick nystagmic movement, not only is the nystagmus more marked, but 
the severity of the vertigo and the sense of rotation are greatly increased. 
It has been noted (Jansen, Barany, and others) that the patient frequently 
assumes a characteristic position in bed,— i.e., he lies with the sound ear 
buried in the pillow, so that, when tempted to look about the room, the 
movement of the eyes will be in the direction of the slow eye motion, which 
position tends to lessen not only the nystagmus but also the distressing 
subjective symptoms. 

Ataxia .—If the patient stands or is supported in the upright position 
with head erect, he exhibits marked disturbance of equilibrium, and falls 
or tends to fall toward the diseased ear. Supposing, for example, that 
the lesion is an acute suppurative invasion of the right ear, the nystagmus 
will be to the left' and the patient will fall to the right. If he turns his face 
toward the right shoulder, thus changing the plane of the nystagmus, he 
will fall backward. If his face is turned toward the left shoulder, he will 
fall forward. 

The pointing reactions in the acute stage of a diffuse suppurative 
labyrinthitis are those invariably present during active vestibular irri¬ 
tation from any cause. (See Chapter XIV.) 


296 


LESIONS OF THE LABYRINTH 


While the patient lies quietly in bed, the subjective symptoms are minimized, 
and, since any sudden movement of the head tends to increase their severity, 
he soon learns to remain quiet and to resist any unnecessary movement. 

The syndrome above described— i.e., the nystagmus and associated 
vertigo and ataxia—is present at the onset and to some extent throughout 
the acute stage of practically every case of suppurative labyrinthitis. Com¬ 
plete absence of this triad is, therefore, a valid reason for excluding acute 
suppurative labyrinthitis. 

Of other symptoms probably the most constant at the onset is headache 
in some form. Often this takes the form of severe deep-seated earache. 
In other cases the pain is not so localized, but is referred to other parts 
of the head,— e.g., the vertex or occiput. The temperature is probably 
always elevated at the onset, and may rise to 103° or 104° F. On the 
other hand, the writer has seen cases of extensive labyrinthine suppura¬ 
tion in which the temperature at no time exceeded 101° or 102° F. When 
in addition to the characteristic vestibular phenomena there are frequent 
vomiting, high temperature, and severe headache, and these symptoms do 
not show early tendency to amelioration, one is forced to consider the 
possibility of meningeal infection. It must not be forgotten, however, 
that any or all of these symptoms may be present at the onset as a result 
of the labyrinthine lesion alone. 

Cochlear Disturbance; Deafness. —A very brief statement will suffice as 
to the deafness of the acute stage of diffuse suppurative labyrinthitis. 
Usually the deafness is such as to force itself upon the physician’s attention. 
In a case which I had an opportunity of watching from the onset to the 
final recovery, one of the earliest symptoms—apparently synchronous with 
the vestibular phenomena—was the profound deafness of the diseased ear. 
As the patient lay with the sound ear buried in the pillow, her failure to 
notice questions or even sounds originating quite near the diseased ear 
proclaimed its practical loss of hearing power. There was never in this 
case any return of cochlear function. 

Personally, I have never seen an indubitable case of diffuse suppurative 
labyrinthitis in which very marked deafness was absent. Sudden and 
profound deafness is, therefore, an important sign of labyrinthine suppura¬ 
tion, and the retention of a demonstrably useful degree of hearing power 
should in my opinion be given very considerable weight as an indication 
that the labyrinth is not involved in a severe suppurative process. 

When in a case of unilateral labyrinthine disease the deafness is in 
doubt, the most convenient and also the most useful and reliable test is 
by means of words and numbers spoken in rather loud voice close to the 
diseased ear, the function of the sound ear being excluded by means of the 
Barany noise instrument (see Fig. 79 on page 95). 

Caloric Test in Relation to the Acute Stage. —In a typical case of diffuse 
suppurative labyrinthitis, the nystagmus toward the sound ear is due 
not to irritation of the diseased vestibular apparatus, but to sudden 
annulment of its function,—this being equivalent in effect to a direct 
irritation of the sound and now unopposed, vestibular mechanism. Irri- 


CALORIC TEST IN RELATION TO ACUTE STAGE 


297 


gation of the diseased ear with hot or cold water would, therefore, be abso¬ 
lutely without effect upon the spontaneous nystagmus present. Irrigation 
of the sound ear with cold water would temporarily check the nystagmus or 
possibly reverse its direction for a few moments. Irrigation of the sound 
ear with hot water would cause great exaggeration of the nystagmus and 
subjective symptoms present, possibly inducing a paroxysm of nausea 
and vomiting. All or any of these phenomena would be more or less cor¬ 
roborative. The author can not see, however, that this test in the average 
run of cases is in any way essential to a correct diagnosis during the acute 
stage, and its influence upon the course of an acute inflammatory process 
within the labyrinth can not be regarded as free from possibilities of harm 
to the patient. With characteristic signs of vestibular irritation and 
profound deafness, the diagnosis of diffuse suppurative labyrinthitis would 
seem to be clear without recourse to the caloric test. On the other hand, 
with symptoms of vestibular irritation and retention of hearing, it would 
seem obviously unwise to subject the diseased ear to any shock which 
might possibly convert a circumscribed infection into a diffuse suppurative 
labyrinthitis. Unless, therefore, there are atypical or contradictory symp¬ 
toms leaving the diagnosis in doubt, the caloric test is to be advised against 
until the symptoms of vestibular irritation have completely subsided. 

Subsidence of Vestibular Symptoms .—In cases in which no intracranial 
complications occur, the disease runs a fairly characteristic course. The 
symptoms of vestibular irritation usually show rather rapid amelioration, 
and in their abatement follow a fairly definite order. That is to say, the 
vertigo and ataxia regularly subside before the nystagmus. Usually from 
the second to the fourth day the nausea and vomiting are relieved. From 
the third to the fifth day of the attack the vertigo is in many cases so much 
less pronounced that the patient is comparatively comfortable as he lies 
quietly in bed. The nystagmus, however, is still present, and turning the 
eyes voluntarily in the direction of the quick nystagmic movements brings 
a return of the vertigo. Sudden or violent movements of the head also 
induce recurrence. The temperature, which may be rather high at the 
onset,— i.e.j 102° or 103° F.,—usually subsides with the recession of the 
vestibular phenomena. At least this is the usual course in an uncompli¬ 
cated case. Usually by the middle or end of the second week, and in some 
cases sooner, the vertigo is so far relieved that the patient—in the absence 
of course of contra-indicating constitutional symptoms—is able to stand 
without discomfort. Even now, however, sudden or exaggerated head 
movements are apt to induce vertigo and ataxia. Finally, during, or by 
the end of, the third week the spontaneous nystagmus usually completely 
disappears. 

This describes the average, with of course very considerable variations 
in individual cases. The writer recalls one case of very severe and rapidly 
fatal labyrinthine infection in which the vertigo and nystagmus seemed 
completely to have disappeared within a week of the onset. In another 
case of extensive labyrinthine suppuration, which recovered only after 


298 


LESIONS OF THE LABYRINTH 


surgical removal of the labyrinth, the spontaneous nystagmus persisted 
until well into the fifth week. 

The Use of Covered Glasses .—It has been found that vestibular nystag¬ 
mus is more or less controlled, or lessened, when the gaze is fixed upon 
some object within easy visual range. The inhibitory influence of this 
focusing of the vision upon one object is not appreciable during the most 
active stage of the nystagmus, but becomes progressively more noticeable 
as the strength of the eye movements is reduced. Barany, following a 
suggestion of Dr. Hans Abels, makes use of this fact by placing before the 
patient’s eyes a pair of opaque, or covered, spectacles, the surfaces of which 
are so near the eye that the vision can not be focused thereon. By thus 
removing the visual resting point, the nystagmus in many cases becomes 
much more marked. In this way the character of a very slight or rapidly 
diminishing nystagmus may be determined, or one that has apparently 
ceased may again become noticeable. It is well, therefore, in doubtful 
cases,— i.e., in cases in which the presence of spontaneous nystagmus is in 
doubt,—to make use of this device. 

When finally the nystagmus has completely disappeared, the patient 
no longer exhibits any demonstrable symptoms of vestibular irritation. 
We have now to determine whether he has suffered from (a) some form of 
transitory inflammation of the labyrinth which has undergone resolution, 
leaving an intact and functionating organ; or (b) from a suppurative laby¬ 
rinthitis by which the vestibular function has been abolished. It is at this 
stage that the caloric test is of paramount importance. 

Symptoms of Labyrinthine Fistula .—Before leaving the discussion of 
the acute stage, a word should be said about the so-called “fistula test.” 
It is a recognized fact that suppurative labyrinthitis may be established 
with or without the demonstrable presence of a gross defect— -i.e., fistula— 
in the labyrinthine wall. It is also conceivable that defects in the bony 
capsule of the labyrinth may exist, as a congenital condition or even as a 
result of tympanic disease, without giving rise to a suppurative process 
within the vestibule. 

In any case in which vestibular irritability is retained, the presence of 
a fistula leading into the labyrinth may be demonstrated by means of any 
instrument by which the air in the external auditory canal can be alternately 
compressed and rarefied. The best instrument for this purpose is one 
embodying the principle of the Politzer inflating apparatus, but having a 
smaller end piece to fit the orifice of the auditory canal. When this is 
moistened and pressed into the meatus, compression of the bulb condenses 
the air in the auditory canal and tympanum and, if a fistula is present, 
forces air into the labyrinth. When the static labyrinth is still functionat¬ 
ing (i.e., susceptible of irritation), this is regularly followed by nystagmus 
which varies in direction in accordance with the location of the fistula and 
the direction of the resulting endolymph displacement. The nystagmus 
thus induced is usually preceded by a slow movement of the eyes in one or 
the other direction, and this slow movement • corresponds to the slow 


FISTULA TEST: ITS DIAGNOSTIC VALUE 


299 


component of the nystagmus. Compression may result in a single slow 
movement of the eyes and their quick return when pressure is relieved, or 
the preliminary slow excursion may be followed by several characteristic 
vestibular movements lasting some seconds. In the presence of a fistula, 
nystagmus can be induced either by compression or aspiration, which, 
however, give rise to nystagmus in opposite directions. That is to say, 
if compression causes nystagmus to the left, aspiration will reverse this 
direction, giving rise to nystagmus to the right. When no fistula exists, 
this experiment is either negative, or gives rise to very slight, almost 
imperceptible eye movements due presumably to pressure upon the struc¬ 
tures closing the labyrinthine windows. Obviously if the vestibular irrita¬ 
bility is completely lost, this test will give negative results even in the 
presence of a fistula. 

The conditions upon which the compression and aspiration test may 
throw light may be stated as follows: 

1. Chronic suppurative otitis media without labyrinthine infection 
and with intact bony capsule: compression test negative. 

2. Defect (fistula) in bony capsule of the labyrinth, but without infec¬ 
tion of membranous labyrinth; shown by absence of spontaneous symp¬ 
toms of vestibular irritation, plus strong reactions to compression and 

aspiration (caloric irritability normal). 

3. Acute stage of suppurative labyrinthitis with fistula; spontaneous 
nystagmus modified by compression and aspiration experiment. 

4. Presence of fistula in the latent stage of suppurative labyrinthitis: 
shown by negative caloric reaction and very slight, but typical, response to 
compression. In this case one might infer that the vestibular mechanism 
had retained a vestige of functional activity which can no longer be stim¬ 
ulated by heat or cold, but can still react to the stronger mechanical irrita¬ 
tion produced by compression. 

Obviously when the caloric reactions are absolutely negative, the 
absence of response to compression or aspiration can not be regarded as 
disproof of the presence of a fistula, since vestibular irritability may be 
completely abolished. 

Since it is easily conceivable that infective matter may be forced by 
air under pressure from an infected tympanum into an uninfected vestibule, 
it is clear that this test should be used with moderation and care. 

Latent, or Quiescent, Stage of Suppurative Labyrinthitis —This stage 
is sometimes spoken of as “chronic suppurative labyrinthitis,” a term 
which is distinctly misleading, since it seems to imply two varieties of the 
disease, just as in acute and chronic purulent otitis media we have different 
types of tympanic inflammation. But wdiereas acute purulent otitis media 
may run its course from onset to resolution without having passed through 
any of the phases characteristic of chronic middle-ear suppuration, every 
case of diffuse suppurative labyrinthitis must inevitably progress — 
and usually quite rapidly-to the latent stage. The disease is said 
to have reached the latent stage as soon as the symptoms of vestibular 


300 LESIONS OF THE LABYRINTH 

irritation— i.e,, spontaneous nystagmus, vertigo, etc—have completely 
disappeared. 

In the latent stage of the disease, the patient may be up and about, 
and may apparently regain his normal standard of health and strength. 
He may now experience no subjective symptoms referable to the labyrinth 
beyond the deafness and certain defects of orientation to be referred to 
presently. For the time being—though this is by no means invariable 
the aural disease may have resumed the role of a circumscribed lesion 
having no appreciable influence over his general constitutional state. It 
is now of the greatest importance to apply some test by which loss or 
retention of vestibular irritability may be determined. The tests which 
have been proposed for this purpose are: (a) the caloric test, (b) the rotation 
test, and (c) the galvanic test. 

The Caloric Test .—To those who have not made use of this test, a 
word as to the method of applying it may be of service. Since the reaction 
depends wholly upon the temperature of the water, and not in any degree 
upon the force employed, a slow continuous current gives better results 
than a stronger intermittent stream. The fountain syringe is, therefore, 
preferable to any form of hand syringe. Barany takes care that the water 
shall be at 30° C. (86° F.), having found that this temperature gives a 
positive reaction in the great majority of cases. There are some cases, 
however, in which no satisfactory reaction follows irrigation with water at 
this temperature. In such cases, reducing the temperature to 75° or 65° F. 
may induce a quick and positive reaction. The disadvantage of using 
very cold water is the greater likelihood of causing nausea and vomiting. 
We should watch carefully for the first appearance of nystagmus. To con¬ 
tinue the irrigation after the nystagmus is clearly established adds nothing 
to our knowledge of the condition and will be likely to cause nausea and 
vomiting. Using water at about 86° F., the average time required to pro¬ 
duce nystagmus is about 40 seconds. There are, however, great variations 
within the physiological limits,— i.e., from 10 seconds to as much as 3 
minutes. The slowest reaction in a presumably normal labyrinth which 
has come under the writer’s personal observation was a case in which the 
nystagmus appeared after two minutes and fifty seconds of continuous 
irrigation. 

As with all forms of vestibular nystagmus, the eye movements are most 
marked, and therefore first become noticeable, when the eyes are turned 
in the direction of the quick nystagmic movement. It is, therefore, well 
to direct the patient to keep the eyes turned in the direction of the ear not 
irrigated when cold water is used and to look toward the ear irrigated when 
hot water is employed. In a case of normal caloric reaction, the nystagmus 
has an average duration of 2 minutes,—differing in this respect from the 
nystagmus following the so-called rotation experiment, the average dura¬ 
tion of which is about 40 seconds. 

Instruments which facilitate the experiment—especially when one is 
working without an assistant—are Barany’s “fixator” for holding the 


CALOEIC TEST: ITS DIAGNOSTIC VALUE 


301 



gaze in the desired direction, and a self-retaining basin for receiving the 
return flow of water (see Fig. 179). An ordinary stop watch is convenient, 
and, if one would be exact, almost essential for determining the quickness 
of the reaction and its subsequent duration. 

It is in the latent or quiescent stage of the disease that this test is of 
the greatest value, leading logically to one or other of two conclusions: 

1. If the caloric test is fol¬ 
lowed by a normal reaction, one 
may infer quite confidently 
that the labyrinth has been in¬ 
volved in a comparatively simple 
process, which, while sufficiently 
severe to have annulled tem¬ 
porarily vestibular irritability, 
has undergone resolution, leaving 
the vestibular apparatus intact. 

Prognosis favorable. 

2. If, on the other hand, the 
caloric test evokes absolutely no 
response, one may conclude with 
equal certainty that the labyrinth 
has been involved in a suppura¬ 
tive process which has either (a) 
actually destroyed the essential 

structures of the membranous 
vestibule, or (b) has inflicted Fig. 179.-Barany’3 fixator and B elf-retainmg basin. 

upon them such injury as to 

have abolished the vestibular function. While this describes a condition 
in which the patient may go for long periods or even indefinitely without 
alarming symptoms, there is no possible assurance of such immunity, 
and the prognosis as to the ultimate outcome can not be regarded other¬ 


wise than with anxiety. 

Rotation Tost .—We have seen that wiio-i a normal person seated with 
head erect upon a revolving chair is turned rapidly in either direction, 
there results when the rotations are suddenly stopped a horizontal nys¬ 
tagmus in the direction opposite to that in which he w r as turned. The 
average duration of this “ after-nystagmus is about 40 seconds. Wliile 
this duration varies considerably within physiological limits, the duration 
of the nystagmus resulting from rotation in opposite directions is usually 
about the same,— i.e., shows a difference of not more than 3 or 4 seconds. 
The diagnostic value of this experiment depends, therefore, entirely upon 
a comparison of the duration of the “after-nystagmus” in opposite direc¬ 
tions. If, for example, an individual is turned ten times to the left and 
exhibits an “after-nystagmus” to right lasting 30 seconds, while ten rota¬ 
tions to the right result in a nystagmus to the left lasting but 15 seconds, 
the inference, so far as we may draw one from this experiment, is that his 







302 


LESIONS OF THE LABYRINTH 


left vestibular apparatus is non-irritable, i.e ., that its function is destroyed 

or abolished. . 

Reducing this to a formula, we may say that great shortening of the 

rotation after-nystagmus in one direction as compared with that in the opposite 
direction points to a non-functionating labyrinth on the side toward which 
the shortened nystagmus is directed. 

One can understand the rationale of this test only by reverting to 
Ewald’s experiments. Ewald found by his experiments on pigeons that in 
either horizontal canal an endolymph movement toward its ampulla induced 
head and eye movements (nystagmus) much stronger than those caused by 
endolymph movement toward the small end of the canal. Barany believes 
that the same is true of human beings, and that the horizontal nystagmus 
to the right following rotation to the left is due in the proportion of two- 
thirds to the endolymph movement in the right canal toward its ampulla, 
and one-third to the endolymph displacement in the left canal toward its 
small end. It is clear, therefore, that if the right vestibule be destroyed, 
the nystagmus to the right following rotation to the left will be reduced by 
two-thirds, while the nystagmus to the left following rotation to the right 
will be reduced only by one-third. Therefore the duration of the nystag¬ 
mus toward the destroyed labyrinth will be only half that toward the sound 
ear. Careful examination of the accompanying diagrams with the explana¬ 
tory notes will, it is believed, make these points and their diagnostic signifi¬ 
cance clear. 



Fig. 180.—Horizontal section of skull passing 
through both horizontal semicircular canals. Ny¬ 
stagmus during rotation to right, (x) axis of 
rotation. Large arrow (o), direction of rotation; 
small arrow (c), direction of endolymph displace¬ 
ment caused by rotation to right; medium arrow 
(6), direction of nystagmus during rotation. Dur¬ 
ing rotation to right there is horizontal nystag¬ 
mus to right. 


Fig. 181.—Nystagmus during rotation to left, 
(x) axis of rotation. Large arrow (a), direction 
of rotation; small arrow (c), direction of endo¬ 
lymph displacement caused by rotation to left; 
medium arrow (6), direction of nystagmus during 
rotation. During rotation to left there is horiion- 
tal nystagmus to left. 




























Fig. 182. —After-nystagmus (i.e., immediately 
following rotation to right), both labyrinths being 
sound, (x) axis of rotation. Large arrow (a), 
direction of rotation suddenly checked at A; 
small arrow (c), reversed direction of endolymph 
displacement when rotations are suddenly checked; 
medium arrow (b), direction of reversed or after¬ 
nystagmus. Force and duration of this after¬ 
nystagmus are due to endolymph displacement in 
the two canals in the following proportion: by 
two-thirds to the endolymph displacement in the 
left canal toward its ampulla, and by one-third 
to the displacement in the right canal toward 
its small end. 


Fig. 183. —After-nystagmus (i.e., immediately 
following rotation to left), both labyrinths be¬ 
ing sound, (x) axis of rotation. Large arrow (a), 
direction of rotation suddenly checked at A ; 
small arrow (c), reversed direction of endolymph 
displacement wdien the rotations are suddenly 
checked; medium arrow (b), direction of reversed 
or after-nystagmus. Force and duration of this 
after-nystagmus are due to endolymph displace¬ 
ment in the two canals in the following proportion: 
by two-thirds to the endolymph displacement in 
the right canal towmrd its ampulla, and by one- 
third to the displacement in the left canal toward 
its small end. 




R 


Fig. 184.—After-nvstagmus (i.e., immediately 
following rotation to right), right membranous 
canal having been destroyed by disease, (x) axis 
of rotation. Right canal (solid black) destroyed 
by disease. Large arrow (a), direction of rotation 
suddenly checked at A; small arrow (c), direction 
of endolymph displacement when rotations are 
suddenly checked; medium arrow ( b ), direction 
of after-nystagmus. Force and duration of after¬ 
nystagmus are due to endolymph displacement in 
left canal toward its ampulla, and represent two- 
thirds of the normal force; right canal, usually 
supplying one-third, having been eliminated by 
disease. 


Fig. 185.—After-nystagmus (i.e., immediately 
following rotation to left), right membranous 
canal having been destroyed by disease, (x) axis 
of rotation. Right canal (solid black) destroyed 
by disease. Large arrow (a), direction of rotation 
suddenly checked at A; small arrow (c), direction 
of endolymph displacement in left canal when 
rotations are suddenly checked; medium arrow 
(6), direction of after-nystagmus. Force and dura¬ 
tion of after-nystagmus are due to endolymph 
displacement in left canal toward its small end, 
and represent therefore only one-third of the nor¬ 
mal force; right canal, usually supplying two- 
thirds, having been eliminated by disease. 


Therefore, the after-nvstagmus toward the right is of only half the duration of that toward the left, 
showing loss of function in the right vestibular apparatus. 














































DEMONSTRATION OF ROTATION TEST 


303 


The key to the diagnostic significance of the rotation test is found in 
Ewald’s theorem that in either horizontal canal endolymph displacement 
toward the ampulla causes much more forcible movements (nystagmus) 
than a similar displacement toward the small end. Barany accepts this 
fact and assumes that in man the influence of an endolymph movement 
toward the ampulla as compared with a displacement in the opposite 
direction is as 2 to 1. 

The diagnostic value of the rotation test is greatest just after the 
symptoms of vestibular irritation have disappeared,— i.e. in the very 
early period of the latent stage. In suppurative labyrinthitis of long 
standing its significance and value are lessened by the fact—now rapidly 
gaining recognition—that as the organism gradually becomes accustomed 
to dependence upon one vestibular apparatus, the after-rotation nystag¬ 
mus toward the destroyed or paralyzed labyrinth gradually approaches 
and finally equals that toward the sound labyrinth. 

In the writer’s opinion, the rotation test is altogether secondary in 
diagnostic importance to the caloric test, but it is nevertheless of some 
value as a corroborative test. It can be applied much more quickly than 
the caloric experiment, and its effects, so far as the patient’s discomfort 
is concerned, wear off much more rapidly. 

The galvanic test differs from the caloric and rotation tests in the follow¬ 
ing particulars,—viz., that, while the latter two give rise to vestibular 
phenomena as a result of endolymph displacement in one or other set of 
co-active semicircular canals, the nature of galvanic irritation is unknown, 
or at best conjectural. It is applied in the following way: One electrode 
being held in the patient’s hand, the other is applied against the mastoid, 
or in front of the tragus, of the ear to be examined. With the cathode in 
contact with the ear, there results a rotary nystagmus in its own direction, 
— i.e., toward the ear experimented upon. When the anode, or positive 
electrode, is held against the ear, a rotary nystagmus in the direction of the 
opposite ear results. These are the normal reactions, and it has been com¬ 
puted (MacKenzie) that a current strength of 4 ma. should induce the 
reaction when the labyrinth is intact and normal. Taking this as a stand¬ 
ard of normality, the advocates of this test (Vlaclvenzie, Alexander) 
claim that the requirement of a current strength of more than 4 ma. is to 
be regarded as an evidence of diminished vestibular irritability. This 
standard has not, however, been generally accepted by students of vesti¬ 
bular disease, and the reports of different observers as to the results of 
galvanic irritation both in health and disease have been so contradictory 
as to leave its practical diagnostic value in considerable doubt. 

Vertigo of Vestibular Paralysis. 12 —I have described the latent stage of 
suppurative labyrinthitis as that in which all symptoms of vestibular 
irritation a re absent. Even after the vertigo of vestibular irritation has 

12 So far as the writer knows, he was the first to describe this phase of suppurative 

labyrinthitis and to include it among the regular manifestations of the latent stage of 
the disease. Vertigo of Vestibular Paralysis: Transactions Am. Otolog. Society, 1911. 



304 


LESIONS OF THE LABYRINTH 


subsided, however, the patient may experience considerable inconvenience 
as a result of the loss of orientation sense, or knowledge of the position of 
his body in space, which the intact vestibular organs confer. 

Orientation .—It is clear that the power of maintaining one s equilibrium 
in all customary positions of the body depends upon what is called, orienta¬ 
tion, or the subconscious knowledge of the position of the body in space. 
If through accident, or attempting the unusual, the body is thrown into 
positions in which its usual relations to the three planes of space are re¬ 
versed, orientation becomes defective or insufficient, and the subjective 
disturbance known as vertigo results. Again, if the faculty of orientation 
is suddenly disturbed or ablated, the individual at once loses his sense of 
stability in space, or in other words experiences vertigo. Obviously the 
vertigo of vestibular paralysis is the vertigo of defective orientation. 

That the vestibular organs can not be regarded as the essential organs 
of orientation is shown by the fact that after removal of one or both laby¬ 
rinths, the individual regains in time his equilibrium. There must be, 
therefore, other contributory factors, and these are found in the muscular 
and arthrodial senses, the tactile sense, and the sense of sight. 

R. T. Slinger and Sir Victor Horsley 13 published in 1906 the results of 
some very interesting investigations, the purpose of which was to measure 
the approximate accurac}' of the muscular and arthrodial senses in what 
they called topognosis, or “the orientation of points of space.” These 
experiments were carried out in the following manner: The person ex¬ 
perimented upon is blindfolded, and before him is held a glass plate gradu¬ 
ated in squares of a half centimetre each. The plate being placed in one of 
the three planes of space,—let us say the sagittal-vertical,— i.e., a vertical 
plane bisecting his body anteroposteriorly,—the left hand is passively 
moved in different directions and the tip of its forefinger then brought in 
contact with some point upon the plate. He is then directed to bring the tip 
of the right forefinger to a corresponding point upon the opposite surface 
of the plate. It is obvious that in this test no information is gained through 
his tactile sense, which would convey the same impression wherever the 
finger might rest. Sight is eliminated by the blindfolding of the individ¬ 
ual. Orientation must, therefore, be chiefly attributed to the muscular 
and arthrodial senses. This experiment was repeated with a large number 
of normal persons. It was found that there is a physiological or normal 
variation, or error, which varied greatly according to the position of the 
plate in relation to the body. Thus, with the plate held immediately in 
front of him in the vertical anteroposterior plane of the body and at a 
height about on a level with the lower end of the sternum, the average 
physiological variation or error was found to be l l /i to 1J4 centimetres. 
As the plate, still in the same vertical plane, is gradually elevated,— e.g., 
first to a level opposite the neck, then opposite the head, and lastly above 
it,—the average error of orientation shows progressive and very rapid 

13 R. T. Slinger and Sir Victor Horsley: Orientation of Points of Space, Brain, 
April, 1906. 







COMPLEX MECHANISM OF ORIENTATION 


305 


increase. From these variations the investigators concluded that “there 
is a progressive diminution of knowledge of space as we pass outward from 
the central axis of the body.” 

These experiments were repeated with 22 adolescent or young adults 
who had become totally and permanently blind in early childhood, and 
with this interesting result,—viz., that the blind subjects exhibited similar 
errors, which also varied in accordance with the level or height at which 
the plate is held; but the errors were distinctly smaller, the average error 
being less by one-fourth than the average error of people with normal 
eyes. From this they concluded, that, “if the information gained by sight 
is permanently blotted out, the muscular sense under necessity can by 
education be brought to a point at least one-fourth better than that learned 
by the normal person.” 

The above experiments have an important bearing upon the compen¬ 
satory power of one part of the mechanism of orientation to assume the 
work of another part whose function is annulled. We have seen that in 
the normal man orientation is a complex function in which the vestibular 
apparatus, the muscular, arthrodial, and tactile senses, and sight, all take 
part. When sight is lost, muscular and arthrodial impressions become more 
sensitive and accurate. When one vestibular apparatus is destroyed, the 
opposite labyrinth must become accustomed to unopposed, unilateral ac¬ 
tive, and the muscular, arthrodial, and tactile impressions of space and 
position must be immensely increased. Until this process of involuntary 
education is well advanced, it is not surprising that the individual experi¬ 
ences occasional vertigo and ataxia, though he does not exhibit nystagmus 
and may show no constant tendency to fall in any given direction. 

Clinical Manifestations of Vestibular Paralysis .—We know that the 
onset of diffuse suppurative labyrinthitis or the removal of one labyrinth 
is invariably followed by very severe vertigo and disturbances of equilib¬ 
rium—these symptoms being the result of hyperactivity of the sound, 
unopposed labyrinth. After these symptoms of vestibular irritation have 
completely subsided, the patient is comparatively comfortable. He has 
now passed the stage when sudden movements of the head cause nystag¬ 
mus and its attendant phenomena, and may be up and walking about his 
room. On getting out of bed in the morning, however, and on making any 
sudden and pronounced changes in the position of his body,— e.g., as in 
stooping over to pick up something from the floor, or even on suddenly 
rising from the sitting posture,—he becomes momentarily dizzy, and may 
even require support to prevent his falling. These symptoms are due solely 
to defective orientation, and, though at first occurring frequently, are very 
slight as compared with the constant and distressing rotary vertigo of the 
acute stages. The attacks rapidly grow less pronounced, and may appar¬ 
ently cease within a few days, so that the patient is led to believe himself 
cured. He is likely, however, to experience a severe recurrence on attempt¬ 
ing any physical act to which he has not reaccustomed himself. For ex¬ 
ample, when he first attempts to walk down an inclined plane,— e.g., in 
20 


306 


LESIONS OF THE LABYRINTH 


going down stairs,—he may experience sudden and severe vertigo, due to 
the sudden call upon his still defective faculty of orientation by this new 
situation; and this may cause him to fall. Having had this experience, he 
calls into compensatory activity certain other senses, chiefly the muscular 
and arthrodial senses and the sense of sight,—and soon learns to go up and 
down stairs without fear or danger. Again, when he first attempts to walk 
in the dark,— e.g., in getting out of bed at night, he may lose all sense of 
direction and may fall, and now must relearn to maintain his equilibrium 
without the aid of sight. 

All the above manifestations of impaired orientation in the latent 
stage of suppurative labyrinthitis were demonstrated in the single case of 
a young physician who was under the care of Dr. A. B. Duel. The same 
patient, having relearned many of the common acts, such as stooping over, 
going up and down stairs, etc., was strolling along the street, and suddenly 
looked up at a tall building then in the process of erection. This deprived 
him of his sense of position or balance and he fell backward. 

Even more typical of the vertigo of vestibular paralysis was a case 
which came under my care at the Manhattan Eye and Ear Hospital some 
years ago. The patient, a man of 28 years, had contracted syphilis seven 
or eight months previously, and some five weeks before I first saw him 
had become suddenly and absolutely deaf, first in the left and then in the 
right ear. 

Examination revealed the following conditions: Both drum membranes 
practically normal; absolute deafness of both ears, both by aerial and by 
bone conduction. Caloric reactions absolutely negative. The patient, 
seated upon a revolving chair, was rotated rapidly first in one direction 
and then in the other, with perfectly negative results,— i.e., there was no 
nystagmus, and the patient experienced absolutely no vertigo or discom¬ 
fort. Clearly we had to deal with a patient both of whose labyrinths were 
absolutely non-functioning and non-irritable. Yet this patient complained 
as much of vertigo as of the deafness. Tests of his equilibrium demon¬ 
strated a type of ataxia presenting the following interesting contrasts 
with the ataxia of vestibular irritation: He walked with marked unstead¬ 
iness,— i.e., with a somewhat tottering gait, keeping his eyes persistently 
on the ground before him. Asked why he looked on the ground he said, 
'‘to keep from falling/’ Yet he was able to keep a straight course and 
walked wherever his will directed. With eyes closed and feet approximated 
(Romberg), he was able to stand steadily. In walking with eyes closed, 
his unsteadiness was greatly exaggerated, but he still contrived to main¬ 
tain a fairly straight course. 

As differentiating the ataxia in this case from that characteristic of 
vestibular irritation, this patient exhibited no nystagmus, complained of 
no sense of rotation, showed no tendency to fall in any given direction. 
He walked laboriously and with some difficulty, compelling his muscles to 
carry him where his will and sight directed. 

The patient was admitted as a ward patient, where his symptoms were 


MANIFESTATIONS OF VESTIBULAR PARALYSIS 


307 


studied by some of my colleagues as well as myself. He never showed 
any signs of returning hearing, but his improvment in orientation was 
progressive and marked, so that when I last saw him, his gait presented 
no peculiarities which would attract the casual observer. In this he 
illustrated the rapid development of the muscular and arthrodial senses 
under the spur of necessity. 

It sometimes happens that a case studied carefully at the time presents 
symptoms which are correctly interpreted only in the light of later expe¬ 
rience. I mention by name such a patient, because her case was carefulh r 
studied by some of my hospital associates. Selena Miller, a girl then of 
14 years, was admitted to the Manhattan Eye and Ear Hospital in Novem¬ 
ber, 1908, with the following history. Four months previously a radical 
operation was performed on the right ear by a competent surgeon. The 
suppurative process had not been relieved thereby, and she had been re¬ 
admitted to the hospital on account of failing health and atypical symp¬ 
toms of disturbed equilibrium. In the hospital she rapidly lost strength 
and flesh, and soon became rather apathetic and practically bed-ridden. 
When induced to get out of bed, she could not walk without support. 
Support being withdrawn, she was apparently unable to maintain her 
equilibrium and would fall. There was no constancy in the direction of 
her falling, and the character of her ataxia seemed so atypical that she 
was suspected of being a quasi-malingerer. On careful re-examination 
of the ears, it was found that the right ear was absolutely deaf and gave 
no response to the caloric test. Operative exposure of the old wound 
revealed a fistula leading into the horizontal canal and granulations pro¬ 
truding from the open oval window. Following an operation providing 
free drainage from the labyrinth, she made a fairly rapid recovery with 
relief of all ataxic symptoms. 

The interesting feature in this case was the peculiar and excessive 
form of ataxia, which can be satisfactorily explained only on one hypothe¬ 
sis: She had suffered suppurative destruction of one labyrinth; she was a 
delicate girl, and the effect of a rather prolonged illness had been to reduce 
to an unusual and remarkable degree her muscular force and control. 
In the latter condition, her muscular and arthrodial senses were so far 
below par as to have failed utterly in compensating for the disturbed 
labyrinthine balance. Hence the patient’s inability to stand or walk, and 
her liability to fall in any direction according to the chance position of the 
body. The disappearance of the ataxia can not in this case be logically 
ascribed to the removal of the diseased and already non-functionating 
labyrinth, but rather to the relief of an extensive suppurative process, 
elimination of which enabled the patient to regain her muscular strength 
and tone, and her muscular and arthrodial senses to resume their role in 
the complex function of orientation. 

The following case, which is the last I shall refer to in this connection, 
was in no wise unusual clinically. It will, therefore, serve the better to 
illustrate the point I wish to make,—viz., the great importance of recog- 


308 


LESIONS OF THE LABYRINTH 


nizing these defects of orientation and their resulting phenomena as be¬ 
longing logically among the late clinical manifestations of the disease. 

L. M., 34 years of age, a carpenter, was admitted to the Manhattan Eye 
and Ear Hospital in May, 1910, suffering from chronic middle-ear suppura¬ 
tion plus chronic suppurative labyrinthitis of the left ear. The labyrinth 
lesion was of long standing and the ear absolutely deaf and quite irrespon¬ 
sive to the caloric test. For this a combined radical and labyrinth exente¬ 
ration was performed. The immediate result of the operation proved that 
the static labyrinth was not wholly non-functionating, for he suffered a 
few days of characteristic vestibular symptoms,— i.e., rotary nystagmus, 
vertigo, etc. These quickly subsided, and the patient was soon up and 
about, and left the hospital to continue treatment in the dispensary. Some 
two months after the operation, while still under treatment for a slight 
discharge, the patient stated that he was in need of money and asked if he 
could take up his work as a carpenter, stating that he felt perfectly fit. I 
told him to do so, only cautioning him to make no arrangements which 
would prevent him coming regularly for treatment. The patient was a 
light-hearted, optimistic Italian, but when I next saw him he was deeply 
despondent. He told me that he had arranged to take up his work, but had 
been obliged to surrender it by the frequent attacks of dizziness which 
overcame him. 

I had little difficulty in assuring him that his trouble was only tempo¬ 
rary and would assuredly wear off in time. But while reassuring him, I 
had time to consider the rather serious possibilities of such a case. Suppose 
that this man had been a builder’s employee whose occupation required him 
to perform his work while standing upon a scaffold suspended high in the 
air. It is not difficult to imagine what might have resulted from an attack 
of vertigo for which he would have been wholly unprepared. Suppose that 
we are called upon to operate for diffuse labyrinthine suppuration upon a 
boy, and, after all spontaneous symptoms have passed, allow him to 
resume the practice, dear to most boys, of diving into the river or swim¬ 
ming pool. May he not drown before he can recover from the ataxia 
dependent upon a sudden disturbance of orientation? 

The type of vertigo which I have endeavored to describe naturally 
shows some variation in different individuals. Ordinarily induced only 
by unusual demands upon the disabled mechanism of orientation, there are 
undoubtedly individuals whose muscular and arthrodial senses are far 
below the normal average of efficiency and who after destructive labyrin¬ 
thitis logically experience for a considerable period a mild grade of vertigo 
and ataxia of more or less constant type. 

To recapitulate: The point I wish to emphasize is that there are two 
distinct forms of labyrinthine vertigo and associated ataxia,—one the 
familiar spontaneous type, due to vestibular irritation and occurring only 
during the acute stage of suppurative labyrinthitis; and the other not 
spontaneous, not constant, not necessarily accompanied by nystagmus, 
characteristic only of the latent, or quiescent, stage of the disease, and 


MANIFESTATIONS OF VESTIBULAR PARALYSIS 


309 


induced solely by sudden and unexpected calls upon the lost or defective 
orientation sense, in the maintenance of which the intact vestibular organs 
are normally so important a factor. This type of vertigo is usually 
wholly relieved in time as other senses are trained to compensate completely 
for the lost or impaired vestibular function. 

Terminations; Prognosis. —Diffuse suppurative labyrinthitis may 
become quiescent and, having permanently destroyed the hearing and 
the vestibular function, may in some cases undergo gradual resolution,— 
possibly by obliteration of the infected labyrinthine cavities by deposition 
of new connective tissue. On the other hand, the suppurative process may 
remain quiescent during many years and then give rise to a rapidly fatal 
intracranial infection. 

Complications .—The pathways of intracranial infection are (a) from the 
cochlea by way of the cochlear nerve channels into the internal auditor}^ 
meatus; (b) by way of the aquaeductus cochleae to the subarachnoid space; 
and (c) from the vestibular cavity by the aquaeductus vestibuli. By far 
the most frequent intracranial complication of suppurative labyrinthitis is 
meningitis; then come cerebellar abscess, sigmoid sinus infection, and lastly 
cerebral abscess. A certain percentage of cases of diffuse suppurative laby¬ 
rinthitis give rise, even before the acute stage is passed, to fatal meningitis. 
Probably the majority of recognized cases reaching the latent stage are now 
operated upon. There are at present, therefore, no available statistics by 
which we may determine what percentage of cases of latent suppurative 
labyrinthitis, not subjected to operation, give rise to intracranial disease. 
Of this, however, there can be no doubt,—viz., that a patient who presents 
symptoms of chronic suppurative otitis media plus symptoms of past 
suppurative invasion of the labyrinth, harbors a lesion which places his 
life in more or less constant danger. 

Circumscribed Suppurative Labyrinthitis. — Circumscribed infection 
of the labyrinth can be said to exist only when one or other main division 
of the labyrinth can be shown to have escaped serious involvement. Thus 
a suppurative process confined either to the cochlear or to the vestibular 
portion would come under this head. Theoretically, an infection of the 
cochlea, not reaching the vestibule, should provide an occasional example 
of circumscribed labyrinthitis, but it is a fact, abundantly established by 
clinical experience, that primary invasion of the cochlea rarely remains 
localized, but tends rather to rapid infection of the entire labyrinth (diffuse 
suppurative labyrinthitis). The static labyrinth, on the other hand, is 
sometimes invaded by a suppurative process which does not spread to the 
cochlea. Just why a suppurative lesion in this portion of the labyrinth 
more frequently remains localized is not easily determined. Probably 
these circumscribed lesions have their inception in a gradual destruction 
of the bony wall of one or other semicircular canal, most frequently the 
horizontal,—resulting in a fistula at this point; it is possible that the grad¬ 
ual progress of this process is accompanied by a surrounding subacute 
inflammation, by which adhesions are formed, and it may be that such 


310 


LESIONS OF THE LABYRINTH 


adhesions act as a limiting barrier to the spread of the destructive lesion to 
the labyrinthine spaces beyond. However this may be, I believe that 
circumscribed suppurative labyrinthitis may in almost every case be de¬ 
fined as a suppurative lesion confined to the vestibular apparatus. 

Symptoms. —The most typical examples of circumscribed suppurative 
labyrinthitis are probably found in cases in which infection has taken 
place through a necrotic defect in the outer wall of the horizontal semi¬ 
circular canal. The symptoms of the onset and acute stage are precisely 
similar to those characterizing the acute stage of diffuse suppurative laby¬ 
rinthitis. That is to say, the onset is announced by spontaneous nystagmus, 

• usually rotary and toward the sound ear, and by vertigo and ataxia, cor¬ 
responding in type to the form of nystagmus present. The hearing, how¬ 
ever, remains fairly good or is only moderately impaired. This preserva¬ 
tion of cochlear function is in reality the differential point between the 
circumscribed and diffuse lesions. 

The manifest symptoms of vestibular irritation undergo progressive 
amelioration and may completely subside within ten days to two or three 
weeks. The patient now presents no conspicuous vestibular symptoms, 
having reached the latent stage, corresponding to the latent or quiescent 
stage of diffuse suppurative labyrinthitis. 

The acute symptoms having subsided, it becomes necessary to investi¬ 
gate the condition of the static labyrinth. Usually the caloric reactions 
are quite negative. In this case the rotation test usually shows greatly 
shortened after-nystagmus in the direction of the diseased ear. In certain 
cases, however, there is a partial recovery of vestibular irritability, the 
caloric tests being followed by reactions of diminished force and short¬ 
ened duration. When vestibular irritability is completely absent, there 
is usually no return of vestibular symptoms; whereas with partial restora¬ 
tion of caloric irritability, the patient is not infrequently subject to very 
distressing attacks of recurrent vertigo. There is always a possibility 
in these cases that the hearing, though not profoundly affected at the 
time of the acute symptoms, may later undergo gradual and very pro¬ 
nounced impairment. 

It must not be implied from the brevity of this discussion that a sup¬ 
purative process confined to the vestibular apparatus is not a very serious 
lesion. Obviously, such a lesion may at any time spread to the cochlea. 
It may also give rise to meningeal infection. There can be no question, 
however, that so long as the cochlea escapes infection, the danger of serious 
intracranial involvement is distinctly less imminent than when the cochlea 
is also diseased. For this reason, and in order that every rational effort 
may be made to prevent its conversion into a diffuse suppurative labv- 
rinthitis, it is of great importance that the circumscribed nature of the 
lesion should be determined as early as possible. 

Diffuse Serous Labyrinthitis. As compared with the suppurative form, 
serous labyrinthitis is a rare lesion. As with the former, it occurs during 
the course of a suppurative middle-ear lesion. With serous as with diffuse 


DIFFUSE SEROUS LABYRINTHITIS 


311 


suppurative labyrinthitis, the symptoms are dependent upon ablation 
or suppression of the vestibular and cochlear functions. During the 
acute stage the symptoms of the two lesions are practically identical, 
and the diagnosis of serous labyrinthitis can not therefore at this time 
be positively made. In the latent, or quiescent, stage, the symptoms 
diverge, from the fact that in suppurative labyrinthitis the loss of vesti¬ 
bular and cochlear function is practically always permanent, while in the 
serous form of the disease resolution is followed by partial or complete 
restoration of function. 

The symptoms of the onset and acute stage are characterized by sudden 
and intense vertigo, with rotary nystagmus, which may at the very start be 
toward the diseased ear, but quickly changes its direction toward the sound 
ear. Nausea and vomiting are also commonly, though not invariably, 
present. Deep-seated earache and headache may be more or less distress¬ 
ing additions to the patient’s discomfort. 

From this short description it will be seen that the difficulties of differ¬ 
ential diagnosis between the serous and suppurative lesions are at this 
stage practically insuperable. It has been claimed (MacKenzie) that 
severe headache, usually present in suppurative labyrinthitis, is commonly 
absent in serous labyrinthitis. The writer has seen, however, cases of 
destructive labyrinthine suppuration in which headache did not at any 
time appear to be an urgent symptom. On the other hand, a sufficient 
number of authenticated cases of serous diffuse labyrinthitis has not yet 
been observed and recorded to enable one with safety to exclude such 
common and easily induced phenomena as headache. The severe form of 
headache occurring during the acute stage of many cases of suppurative 
labyrinthitis which progress favorably— i.e., without serious complica¬ 
tions—is presumably due to hyperaemia or slight serous inflammation of 
the meninges, and there is no reason to believe that the same may not 
occur in the acute stage of a serous labyrinthitis. 

With the subsidence of vestibular symptoms, the disease lapses into a 
latent or quiescent stage quite similar to that described in suppurative 
labyrinthitis. It now becomes possible for us to make a more positive 
diagnosis by means of the usual tests of vestibular function. If the caloric 
tests induce absolutely no response, and a shortened nystagmus toward 
the diseased ear follows rotation, and the negative reaction to these tests 
is repeated after two or three weeks, the diagnosis of suppurative laby¬ 
rinthitis would seem to be positive. If, on the other hand, the caloric 
test shows returning vestibular irritability, the serous character of the 
inflammation may be assumed. 

As before stated, diffuse serous labyrinthitis is, in the light of our 
present knowledge, a comparatively rare disease. The importance of 
distinguishing such a lesion from a suppurative labyiinthitis depends in 
great part upon two facts! (1) Serous labyrinthitis offois a comparati\ el\ 
favorable prognosis, both as to life and the aural function ) and (2) operation 
upon the labyrinth is therefore clearly contraindicated. 


312 


LESIONS OF THE LABYRINTH 


Perilabyrinthitis.— This term is used to describe the condition in which 
the cellular bone surrounding the labyrinthine capsule is acutely inflamed. 
It may occur either in acute mastoiditis, or during acute exacerbations of 
chronic otitis media. Presumably the inflammatory process involving 
the cellular bone surrounding the labyrinth involves also to some extent 
the labyrinthine capsule itself. On this hypothesis, the vestibular symp¬ 
toms may be attributed to intralabyrinthine congestion secondary to the 
inflammatory changes in the bone. The occasional presence with perilaby¬ 
rinthitis of facial paresis or paralysis is presumably due to pressure upon 
the nerve by inflammatory exudates within the facial canal. The lesion 
may undergo resolution after the mastoid or tympanic disease is controlled, 
or ma}^ give rise to serous labyrinthitis or even to diffuse suppurative 
labyrinthitis. 

Symptoms. —In typical cases, the disease is announced by sudden 
attacks of characteristic vestibular vertigo, which may last but a few 
minutes or an hour or more, but which show a marked tendency to recur¬ 
rence. The first attack may be induced by some sudden movement of the 
head, as in stooping low, sudden rising from the recumbent position, etc., 
or it may occur spontaneously,— e.g., during the night, awakening the 
patient from a sound sleep. The accompanying nystagmus is usually of 
rotary character and is commonly directed toward the diseased ear. Hear¬ 
ing during the attack may be moderately or very markedly impaired. As 
the attack wears off, the hearing power improves, and may reach the aver¬ 
age acuteness for the patient. Between the attacks Weber’s test is usually 
referred to the diseased ear (Neumann). During the intervals between 
the attacks the caloric reactions and the reactions to the tuning experiment 
are normal. With the recurrence of the attacks, their character may 
change in that the direction of the nystagmus may be reversed— i.e., may 
be directed toward the sound ear—and the loss of hearing may be much 
more pronounced. Such changes, however, suggest the conversion of the 
lesion into a diffuse labyrinthitis, serous or purulent. According to Fletcher, 
the labyrinthine symptoms in perilabyrinthitis clear up after the tympano¬ 
mastoid lesion has been corrected,— i.e., after a simple mastoidectomy or 
a careful radical operation according to the indications present. 

In reviewing the foregoing pages, it may seem to the reader that the 
dividing line between these lesions is in many cases so indefinite as to be of 
academic interest rather than of practical importance. Thus, a circum¬ 
scribed labyrinthitis may easily become diffuse, a serous labyrinthitis may 
become purulent, and a perilabyrinthitis may give place either to serous 
or to purulent inflammation of the labyrinth. This narrow boundary line 
between the different lesions renders their clinical recognition the more 
important, since the indications for treatment are quite different, and the 
correct diagnosis and management of a comparatively simple lesion may 
preclude the development of one in the highest degree dangerous as to life. 
The more important clinical differences between the four lesions above 
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ACUTE LABYRINTHINE HYPEREMIA 


313 


Acute Hyperaemia of the Labyrinth. — Before leaving the subject 
of acute vestibular disease, a word should be said as to the condition de¬ 
scribed as labyrinthine hyperaemia. Since a direct anastomosis between 
the vessels of the tympanum and those of the labyrinth has not been de¬ 
termined, it is somewhat difficult to explain this condition as secondary 
to tympanic congestion. There are, however, occasional cases of severe 
vestibular vertigo, usually accompanied by loud tinnitus and lasting but a 
few minutes, which are difficult to explain upon any other hypothesis than 
as depending upon temporary changes in the local blood supply or pressure. 

A personal experience of the writer may provide an illustration. Hav¬ 
ing suffered for twenty or more years with bilateral catarrhal otitis media, 

I have never experienced an acute middle-ear lesion. Some fifteen years 
ago, I awoke one morning with what seemed to me the severest form of 
vertigo. Everything in the room swam in circles about me in the hori¬ 
zontal plane. There was a loud roaring sound in my right ear. Y hether 
the hearing was temporarily involved I do not know. The severity cf the 
vertigo was such that it would have been quite impossible for me to have 
stood without support. This vertigo lasted probably ten or fifteen min¬ 
utes,—it seemed much longer,—and then gradually wore off, leaving my 
ears apparently in statu quo. There has never been the slightest recurrence. 
The transitory character of the attack apparently negatives the possibility 
of the smallest hemorrhage or effusion into the labyrinth, and leaves sud¬ 
den temporary hyperaemia as the most plausible theory as to its causation. 
As to the causes of the hypersemia in such cases, we are very much in the 
dark, unless it be due to disturbances of the general circulation combined 
with local changes in the minute labyrinthine vessels. 

While attempts have been made to describe in detail the symptoms of 
acute labyrinthine hypersemia, I know of no recorded series of cases upon 
which data are based. Probably, were a sufficient number of cases brought 
under the care of a competent observer, it would be found that the vesti¬ 
bular phenomena of nystagmus, vertigo, and ataxia are invariably present 
and are co-ordinated according to Barany’s laws, and that when the aural 
disorder is unilateral, the nystagmus is usually directed toward the in¬ 
volved ear. 

Prognosis and Treatment of Diffuse Suppurative Labyrinthi¬ 
tis. —Before taking up in detail the management of infective diseases 
of the labyrinth, there are one or two general facts which deserve brief 
consideration. 

Suppurative labyrinthitis per se is not a fatal malady. If resulting 
fatally, death is caused not by the labyrinthine disease itself, but by some 
intracranial lesion to which it gives rise. The necessity in any case for 
immediate operation must be determined, therefore, not by the evidences 
of vestibular involvement, but by the danger of intracranial infection. If 
our experience, judgment, and diagnostic skill enable us to foretell from 
the physical character of the lesion and its clinical phenomena that menin¬ 
geal infection is threatened or imminent, prompt surgical drainage of the 


314 


LESIONS OF THE LABYRINTH 


labyrinth is clearly the rational and conservative method of treatment. 
On the other hand, if we are able to deduce from the character and course 
of the symptoms a comparative freedom from such danger, early operative 
intervention is often distinctly contra-indicated. 

We now know that in any series of correctly diagnosticated cases of 
labyrinthine suppuration a certain percentage of the patients will survive 
the attack without surgical intervention; that others of the same series 
will prove fatal through extension of the disease to the brain or meninges. 

Hinsberg, from his own personal experience and from an analysis of 
the published records of other surgeons, believes that, of uncomplicated 
cases correctly diagnosticated and operated upon by competent surgeons, 
the mortality will not exceed 2 per cent., while of such cases not operated 
upon the ultimate mortality will reach 10 per cent. A consideration of 
such estimated percentages, and probably the observation of certain cases 
of rapidly fatal meningitis, have led some surgeons to the statement of 
rather hasty conclusions as to the necessity of early operation upon the 
labyrinth in all cases of suppurative labyrinthitis. Thus, Jansen 14 says, “If 
we appreciate the freedom from danger of opening the vestibule, . . . 
we should be able to set up the principle that as soon as labyrinth disease 
has been diagnosticated in one of its principal parts, the (labyrinth) opera¬ 
tion is admissible in every case.” The writer believes that such a dogma 
is not only incorrect in theory, but is likely in practice to lead to operations 
which are in many cases uncalled for, and in others actually dangerous to 
life. The author would emphasize the statement of Neumann, 15 that “not 
every circumscribed labyrinthine suppuration must become a diffuse one, 
for the intact portion of the labyrinth may be protected by firm adhesions 
until the diseased part of the labyrinth shall have entirely and spontane¬ 
ously healed.” 

Clearly the management of these cases calls for careful and skilful 
surgery when surgical aid is indicated; but in even greater degree may the 
patient’s life depend upon the physician’s ability correctly to interpret 
symptoms and to deduce therefrom a correct plan of treatment. 

Diffuse Suppurative Labyrinthitis. — The treatment of this disease 
varies with the stage and also with the type of the attack. It is best con¬ 
sidered, therefore, under different headings. 

I. Typical Uncomplicated Case; Acute Stage. — Symptoms: Nystag¬ 
mus, vertigo, and disturbance of equilibrium; nausea and vomiting; ear¬ 
ache, headache, moderate fever, absolute deafness of involved ear. 

Treatment: The symptoms at this stage usually confine the patient 
to bed, where he should be kept until all signs of vestibular irritation have 
completely disappeared. The bowels should be evacuated by cathartic 
drugs or by enema. The patient should be placed upon fluid diet, this to 
be replaced by light diet as soon as the condition of the stomach will 

14 Jansen: Trans. Amer. Laryn., Rliin., and Otol. Soc., 1908, p. 136. 

15 Neumann. Infectious Diseases of the Labyrinth, Laryngoscope, November, 





SUPPURATIVE LABYRINTHITIS 


315 


permit. He should be advised and guarded against any unnecessary 
movements. He should not be allowed to get out of bed in order to go to 
the closet or for any other purpose. No attempt should be made at this 
time to investigate his control of static equilibrium. In the author’s 
opinion, the caloric test should not at this time be applied except in certain 
obscure cases in which it may aid in the differentiation between a possible 
brain or labyrinthine lesion. In typical cases the caloric test adds little 
to our practical knowledge of the condition during the acute stage, and 
may influence the progress of the lesion unfavorably. The cleansing of 
the ear at intervals should be accomplished with the least possible dis¬ 
turbance of the patient. In a word, he should be subjected to no measures 
of examination or treatment calling for unnecessary movements of the 
head, which invariably add to the severity of the vestibular symptoms. 

The question of operating upon the labyrinth during the acute stage 
of suppurative labyrinthitis should be decided solely by the presence or 
absence of symptoms pointing to danger of intracranial infection. If 
excessive and continuous headache, high fever, mounting rather than 
receding from day to day, frequent and persistent vomiting,—if these 
symptoms by their severity and particularly by their continuance point 
to dangerous meningeal congestion, we may be forced to drain the laby¬ 
rinth in the hope of checking the spread of the disease. 

On the other hand, if the clinical picture does not indicate impending 
intracranial infection,— e.g., if the temperature is normal, or, having been 
elevated, shows progressive, though gradual, recession toward the normal 
line; if the patient is reasonably comfortable, and from day to day becom¬ 
ing more so; and if the symptoms of vestibular irritation are gradually 
subsiding, the writer believes that surgical intervention, for the time being, 
is distinctly contra-indicated, and should not be thought of until all symp¬ 
toms of vestibular irritation have completely subsided. 

II. Diffuse Suppurative Labyrinthitis with Fistula; Acute Stage— Symp¬ 
toms: Phenomena of vestibular irritation (nystagmus, vertigo, etc.) plus 
fistula symptom (nystagmus modified by compression and aspiration 
test); temperature normal or only slightly elevated; absolute deafness of 
diseased ear. 

The treatment is practically the same as for Group I. The presence 
of a fistula of spontaneous development and presumably leading into one 
of the semicircular canals is generally regarded as influencing the prognosis 
favorably (Hinsberg, Panse, Jansen). The labyrinthine operation is, 
therefore, contra-indicated during the acute stage except in the presence of 
symptoms of threatened intracranial disease. 

III. Suppurative Labyrinthitis following Stapedial Injury. —Character¬ 
ized by symptoms of vestibular irritation and profound deafness following 
quickly upon accidental injury to the stapes during a radical or other 
tympanic operation,— e.g., subluxation of stapes, rupture of annular 

ligament, etc. 

Most observers agree that infection of the labyrinth resulting iiom 


316 


LESIONS OF THE LABYRINTH 


surgical injury in the region of the oval window is particularly prone to 
spread rapidly to the brain or meninges. Pus thus admitted reaches the 
vestibule and cochlea before any inflammatory products are formed to 
bar its passage along the minute channels uniting the labyrinthine and 
brain cavities. Such lesions also almost invariably cause absolute and 
permanent deafness. The author, therefore, believes that they constitute 
an exceptional group in which the labyrinth should be opened and drained 
as soon as the diagnosis of labyrinth infection is made. 

As bearing upon the importance of early operation in these cases, the 
statistics of Jansen are of interest. His report 16 included 19 cases of acci¬ 
dental injuries, made during the radical operation, subsequent curette- 
ment, etc. Of these the labyrinth was subsequently opened and drained 
in 13 cases, of which 9 recovered. Of 5 cases in which the labyrinth was 
not operated upon, all died. The extreme gravity of infections of the 
labyrinth resulting from accidental injuries during operation is indicated 
by the total mortality,—viz., 9 out of 19. Jansen’s report is also impres¬ 
sive as showing the importance of care to avoid such surgical mishaps. 

Note. —It should be understood that under Group III the writer includes only 
those cases of traumatic labyrinthitis which result from injuries involving the stapes. 
The accidental opening of the horizontal semicircular canal may not give rise to diffuse 
suppurative labyrinthitis, in which case it belongs to a quite different class. 

IV. Suppurative Labyrinthitis with Meningeal Irritation; Acute Stage .— 
Symptoms of vestibular irritation plus continued high temperature, per¬ 
sistent headache, frontal or occipital, and vomiting. These latter symp¬ 
toms, while not very uncommon at the onset, usually show progressive 
diminution even during the first days of the attack in uncomplicated cases. 
When they persist undiminished, or are increased from day to day, one is 
forced to infer at least meningeal congestion of rather high grade. In 
such cases the labyrinth should be opened and drained and the meninges 
should be exposed in the posterior fossa, i.e., by removing the bony plate 
covering the cerebellar dura from the anterior border of the sigmoid sinus 
forward toward the petrous bone. 

It has frequently been argued that intracranial complications might 
be forestalled by routine early operation,— i.e., early drainage of the laby¬ 
rinth,—as soon as suppurative labyrinthitis has been diagnosticated. 
This argument is invalidated by the fact that the labyrinth operation 
itself may precipitate a spread of infection beyond the confines of the 
labyrinth,— i.e., to the brain or meninges. There can be no doubt that 
this is far more likely to occur when the operation is performed in the early 
days of a labyrinthine attack than when it can be postponed until the 
disease has reached the latent or quiescent stage. 

Latent Stage of Diffuse Suppurative Labyrinthitis— Symptoms: Abso¬ 
lute deafness; absence of caloric irritability; after-rotation-nystagmus 
toward diseased ear only half the duration of that toward the sound ear. 


10 Jansen: Trans. Amer. Laryn., Rhin., and Otol. Soc., 1908. 




TREATMENT OF DIFFUSE LABYRINTHITIS 


317 


Occasional disturbance of equilibrium due to loss of orientation sense. 
Usually persistent aural discharge. 

Treatment : In this condition we have to deal with a lesion which has 
already destroyed the cochlear and vestibular functions. It is a condition 
which imposes a very considerable responsibility upon the physician. If 
he could satisfy himself that the disease had run its course, setting up 
barriers against the further invasion of surrounding structures, it might be 
justifiable to treat such cases expectantly. There are, however, no means 
of determining that such a lesion is, or will remain, so limited. The middle- 
ear disease is still subject to exacerbations, and in any one of these recur¬ 
rent attacks, the already exposed labyrinth may have to bear the brunt. 
I believe, therefore, that the safest method of treatment, and the only one 
which effectually removes a very positive menace to life is by the combined 
radical-labyrinth operation. 

In many cases, aside from the dangers above referred to, the continued 
discharge and the dread engendered by the recent vestibular attack con¬ 
stitute a rather urgent reason for the adoption of some plan offering reason¬ 
able promise of a complete cure. Again the radical-labyrinth operation 
affords the only means to this end. 

Over this question— i.e., whether in a case of diffuse suppurative laby¬ 
rinthitis which seemingly has run its course, leaving a functionally dead 
labyrinth, a radical mastoid operation, if indicated, should always be sup¬ 
plemented by surgical drainage of the labyrinth—there has been a growing 
diversity of opinion. The old dogma of the \ ienna School, that in such a 
case any operation upon the mastoid which does not include surgical 
drainage of the labyrinth subjects the patient to increased danger, now 
finds many dissenters. Many New York surgeons of reputation now hold 
that there are cases in which in the presense of a functionally dead laby¬ 
rinth, with sufficient time having elapsed for the labyrinthine lesion to 
have undergone resolution, and with no pnysical evidences of a labyrinthine 
fistula, one is justified in doing simply a careful radical operation, without 
opening the labyrinth. In support of this view, the fact is adduced that 
certain competent surgeons have opened the labyrinth in such cases with¬ 
out noting anv macroscopic evidences of labyrinth infection, and the 
further fact that many cases have now been treated surgically without 
opening the labyrinth with apparently perfectly satisfactory results. 
These views and the clinical reports on which they are based are certainly 
worthy of careful consideration. Personally I have not up to the present 
time been able to accept in principle the hypothesis on which the above 

treatment is based for the following reasons. 

(1) To withhold operation in the labyrinth because of the absence ot a 
visible defect in the labyrinthine capsule is possibly to overlook the most 
dangerous type of case,— i.e., one in which a latent focus of mtra-laby- 
rinthine infection persists and in which no natural pathway of escape to 

the tvmpanum is present. . 

(2) To operate on the labyrinth only in those cases in which a fistula, or 


318 


LESIONS OF THE LABYRINTH 


necrotic defect, is disclosed during a radical operation, seems illogical 
from the fact that the commonest cases ol demonstrable fistulse— i.e ., in 
the horizontal semicircular canal—are precisely those which are- regarded 
by many competent observers (Hinsberg, Panse) as offering the least danger 
to the patient’s life. 

(3) Assuming in a given case that a radical operation without 
surgical drainage of the labyrinth is quite satisfactory in its im¬ 
mediate results: is the future safety of the patient so well provided for 
or assured? 

(4) There can be no doubt that the latent stage of a diffuse suppurative 
labyrinthitis is the stage in which operative intervention is attended 
with least risk. Is not this risk very small as compared with the 
possibility of a latent focus of intralabyrinthine infection which may 
be rekindled either by *the radical operation itself or by other causes 
later in life? 

(5) Personal Experience .—I have operated on a fair number of cases of 
diffuse suppurative labyrinthitis in the “chronic”, or latent stage, with¬ 
out a single mishap or fatality. Conversely, in a case of chronic suppurative 
otitis media, with a functionally dead labyrinth, in which I performed a 
radical operation without opening the labyrinth, the patient redeveloped 
an active suppurative labyrinthitis which led to the formation of a 
cerebellar abscess, this causing the patient’s death. This patient was 60 
years old, the original invasion of the labyrinth had occurred many years 
previously, and the labyrinth walls showed no macroscopic defect during 
the radical operation. 

The whole question of labyrinthine surgery is one in which dogmatic 
statement should be avoided, since what is safe in one man’s hands is not 
so in another. Any labyrinthine operation by a man who is not sure of his 
anatomy, who has not a clear conception of the mechanical result he wishes 
to accomplish, and who has not been at some pains to develop his technic, 
is necessarily extremely dangerous. There is also a choice of operations as 
involving different degrees of risk. The use of the chisel in the region of 
the labyrinth is surely dangerous. I believe that I have evolved, not a new 
operation, but a simple surgical method of opening an infected labyrinth, 
which in the latent stage involves little or no risk to the patient’s life. On 
the other hand, any operation in the acute stage is attended with danger 
which the method employed cannot eliminate. If we act on a hypothesis 
of supposedly greater conservatism, and operate in a case of latent sup¬ 
purative labyrinthitis without draining the labyrinth, the patient may le- 
cover perfectly. But, if an active labyrinthitis is rekindled, the danger to 
life is many times increased, and operative intervention, if called for, offers 
a much less favorable prognosis. 

Treatment of Circumscribed Suppurative Labyrinthitis.— Acute 
stage characterized by vestibular nystagmus, vertigo, and ataxia, earache, 
normal or moderately elevated temperature, nausea and vomiting at onset. 
Hearing only moderately impaired. 


TREATMENT OF CIRCUMSCRIBED LABYRINTHITIS 319 


The treatment is the same as for the acute stage of diffuse suppurative 
labyrinthitis,— i.e., absolute rest in bed, fluid or light diet, regulation of 
bowels, local cleansing treatment of diseased ear. Operation upon the 
labyrinth is positively contra-indicated except in the presence of rather 
pronounced and persistent symptoms of meningeal irritation. 

Latent Stage .—Circumscribed suppurative labyrinthitis may in the 
quiescent, or latent, stage show clinical differences justifying a division of 
cases into two groups. 

Group I, characterized bv total, permanent loss of vestibular irritability 
(absence of caloric reactions) plus retention of a useful degree ol hearing 
power. 

The conservative treatment of such a case calls for a very careful 
radical operation. The region of the horizontal canal should be closely 
scrutinized for evidences of localized necrosis (fistula). Finding a necrotic 
tract leading toward the vestibule or canals, the diseased bone should be 
carefully removed, an effort being made to avoid injury to the membranous 
labyrinth beyond the area of osseous necrosis. The posterior wound should 
not be closed at the time of the bone operation, the plastic work upon the 
membranous canal being postponed until the site of the fistula has been 
closed or filled in by healthy granulations. 

Should absolute deafness follow quickly upon the bone operation, and 
particularly should symptoms of meningeal irritation supervene, the safety 
of the patient might call for prompt surgical drainage of the labyrinthine 
cavities. 

Should close scrutiny reveal no area of necrosis leading toward the 
labyrinth, the operation should be completed as a very careful radical. 
While this does not cover all possible sources of danger, it contemplates a 
reasonable division of risk, and avoids possible harm to the patient through 
what is sometimes not inappropriately called “meddlesome surgery. 

Group II. —Symptoms: Vestibular irritability diminished but not lost; 
useful hearing power retained. Periods of comparative comfort alternat¬ 
ing with recurrent attacks of vertigo. 

Presumably the lesion is of the nature of a necrotic process which has 
destroyed a limited portion of the membranous vestibular mechanism. 
The patient experiences periods of comparative freedom from vestibular 
symptoms, and again recurrent attacks of vestibulai \eitigo. The ves¬ 
tibular attacks probably correspond with periods in which the vestibular 
lesion is rekindled into fresh activity or into actual advance. Only in 
this way can be explained a class of cases examples of which have come 
under the writer’s observation both in this country and in clinics and 
hospitals abroad. These patients are much more miserable than those 
in whom the vestibular mechanism has been destroyed and its function 
permanently annulled. 

Treatment: Considering the distress and suffering which this condi¬ 
tion imposes upon its victims, and also the dangeis which aie inseparable 
from the recurrent attacks, the writer believes that the only adequate 


320 


LESIONS OF THE LABYRINTH 


treatment is one which, unfortunately, sacrifices the hearing of the dis¬ 
eased earviz., the radical operation combined with surgical drainage of 
the labyrinth. 

Treatment of Diffuse Serous Labyrinthitis. —The treatment of 
serous labyrinthitis can be dealt with very briefly. During the acute 
stage— i.e., while active symptoms of vestibular irritation are present : 
the disease cannot with certainty be differentiated from suppurative 
labyrinthitis, and the treatment is the same as for an uncomplicated case 
of that disease. 

After the vestibular symptoms have completely subsided (quiescent 
stage) the simpler character of the lesion is made known by returning ves¬ 
tibular irritability. Obviously labyrinthine operation is not only uncalled 
for but contra-indicated. It is equally clear that the pre-existing tympanic 
or mastoid disease should be corrected, and for this reason a radical opera¬ 
tion or simple mastoidectomy may be necessary. 

Treatment of Perilabyrinthitis. —Since the symptoms of this 
disorder are dependent chiefly upon acute inflammatory changes in the 
cellular bone surrounding the bony capsule of the labyrinth, the logical 
treatment should be the correction of this underlying cause. In a majority 
of cases the attack is secondary to acute mastoiditis, less frequently to an 
acute exacerbation of chronic suppurative otitis media. Quite recently 
the writer had under his care a typical case, with nystagmus, pronounced 
vertigo, nausea and vomiting, in a patient suffering from acute purulent 
otitis media. This patient made a perfect recovery with no other treat¬ 
ment than incision of the drum membrane and the usual treatment for 
acute middle-ear suppuration. When perilabyrinthitis occurs as a com¬ 
plication of acute mastoiditis, the treatment involves a dual problem,— 
(a) relief of the mastoid lesion, and (b) avoidance of any unnecessary jar, 
or concussion, which might convert a simple labyrinthine congestion into 
an acute inflammatory process leading quickly to diffuse suppurative 
labyrinthitis. 

If the mastoid symptoms are of moderate grade, it is much safer to 
depend for the time upon free incision of the drum membrane and the so- 
called abortive method of treatment described under acute catarrhal 
otitis media, leaving the question of mastoid operation to be decided later. 
Under this expectant plan, it will be found that many cases will make very 
rapid progress toward recovery. It is of course important, however, that 
the physician keep the patient under close observation and be prepared 
promptly to open the mastoid should the symptoms either of labyrinthine 
disturbance or of the lesion within the mastoid become more marked. 

If the mastoid disease itselt is of such a character as to demand prompt 
surgical relief, the greatest care should be observed to avoid any concus¬ 
sion or jar of the temporal bone. It is clearly desirable, therefore, that the 
mallet and chisel should not be used. The best operative method for 
these cases is that described by Dr. W. S. Bryant, by which the mastoid 
tip is first removed by means of a suitable rongeur, the same instrument 



TREATMENT OF PERILABYRINTHITIS 


321 


being used to remove the entire cortex. Entering the mastoid by this 
route, it is perfectly practicable to complete the operation with no other 
bone-cutting instruments than the usual mastoid curettes and rongeurs. 
In America this method of opening the mastoid has become the routine 
practice of many surgeons of note, among whom may be mentioned 
Drs. T. Passmore Berens and Arthur B. Duel, of New York. Bryant’s 
description of this operation is short, clear, and contains a convincing 
statement of its advantages over other methods in certain cases. 17 

To epitomize: While the logical treatment of perilabyrinthitis is 
directed against the surrounding zone of inflammation, the time of prefer¬ 
ence for surgical intervention is the period between labyrinthine attacks. 
There are .cases in which the attack may be aborted, or the lesion con¬ 
trolled, by non-operative measures. When surgical intervention during, 
or closely following, the labyrinthine attack is clearly indicated by the 
urgency of the symptoms it is important that some operative method be 
adopted by which surgical or bone concussion can be as far as possible 
eliminated. 

Differential Diagnosis .—There are few conditions not directly depen¬ 
dent upon aural disease for which suppurative labyrinthitis is likely to be 
mistaken. Cerebellar abscess in certain cases gives rise to rotary nystag¬ 
mus, vertigo, and ataxia, but usually there are differences in the relation 
of these phenomena to each other and to other symptoms present which 
should enable a trained and careful observer to recognize their origin. 
On the other hand, the physician or aurist who has only a superficial 
knowledge of labyrinthine phenomena might easily be led into a mistaken 
diagnosis, and from this to an unfortunate, and perhaps disastrous, error 
in treatment. It is hoped that a careful reading of the foregoing pages 
may be of value not only to students and practitioners of medicine, but 
also to special students of otology, in placing before them a sufficiently 
comprehensive picture of labyrinthine reactions, both in health and dis¬ 
ease, to render such errors unlikely. 

The more important clinical differences between diffuse suppurative 
and other inflammatory lesions of the labyrinth are given in tabular form 
facing page 312. 

The differential diagnosis between diffuse suppurative labyrinthitis 
and cerebellar abscess is of special importance to the student of aural and 
brain surgery. It will be considered in connection with the symptoms of 
cerebellar abscess. 

17 Bryant: The Technic of the Complete Mastoid Operation, Improved, Shortened, 
and Simplified through the Digastric Route, Transactions Am. Otol. Society, 1907. 




CHAPTER XII. 

SYMPTOMS OF INTRACRANIAL DISEASE SECONDARY 

TO AURAL SUPPURATION. 

It is not to be expected that the otologist should bring to the consid¬ 
eration of brain lesions the broad and comprehensive knowledge of the 
trained neurologist. Necessarily, there may be aspects of a given case, 
patent enough to the latter, which escape the former. Yet it is probably 
true that any otologist in large hospital practice is obliged to assume 
responsibilities in the treatment of suppurative brain lesions quite as 
heavy as fall to the lot of the average neurologist. Cases are not unknown 
in which a competent neurologist called to such a case has been able to 
provide theories,—correct so far as they have gone,—but has not felt 
justified in advising the prompt and active intervention necessary to save 
the patient’s life. On the other hand, there have been cases in which the 
surgeon, acting upon his own judgment, has performed exploratory opera¬ 
tions on account of supposed brain lesions which have not been found on 
opening the skull. It is a pity, therefore, that all such cases should not 
come under the careful joint study of specialists in both branches of med¬ 
icine. Unfortunately, the aural surgeon is frequently called upon to act in 
cases in which the patient’s only chance lies in prompt intervention. 

There are then certain suppurative lesions of the brain or meninges 
which will inevitably form part of the aurist’s experience. Mentioned in 
the order of their frequency they would probably come somewhat in the 
following order: (1) extradural abscess, (2) infective sigmoid sinus throm¬ 
bosis or phlebitis, (3) cerebral abscess, (4) leptomeningitis, (5) cerebellar 
abscess. 

In any large series of cases of middle-ear suppuration, these brain 
lesions recur with sufficient frequency to impose a rather heavy responsi¬ 
bility upon the aurist. It may be well, therefore, to devote a few pages to a 
brief preliminary discussion of certain more or less common phenomena— 
including headache, vomiting, pulse changes, temperature changes, local¬ 
ized convulsions, localized paralyses, mental changes, and the different 
forms of aphasia—one or more of which are usually present in every case 
of meningeal or brain infection. 

Headache. —With the exception of infective sinus thrombosis or 
phlebitis, headache in some form is present at some stage of every sup¬ 
purative lesion within the cranial cavity. On the other hand, if we except 
purulent leptomeningitis, in which headache is usually both severe and 
constant, there is no intracranial lesion secondary to middle-ear suppura¬ 
tion in which it may not be absent during very considerable periods. 

Macewen mentions severe headache as a characteristic and invariable 
symptom of the onset, or acute stage, of cerebral abscess. This, however, 
322 


HEADACHE; VOMITING 


323 


is just the stage of intracranial disease which the surgeon most rarely has 
the opportunity to observe. After the abscess is fully formed,— i.e., after 
it has taken the form of a circumscribed subcortical collection of pus,—• 
the excruciating character of the pain usually subsides, giving place to dull, 
indefinite, and in most cases intermittent head pains. The writer has seen 
fatal cases of brain abscess in which for days the patient complained of 
little pain. 

To this extent, then, headache may approach the dignity of a differ¬ 
ential sign,— i.e., in that it is quite often of dull, indefinite, or intermittent 
character in fully developed cerebral abscess, while in leptomeningitis it is 
usually constant and tends to increasing severity up to the time when the 
patient becomes stuporous or enters upon convalescence (rare). Complete 
absence of headache extending over considerable periods would justify 
the physician in positively excluding leptomeningitis. 

In cases seen by the author, the headache of cerebellar abscess has been 
of distinctly severer and more persistent type than that accompanying 
cerebral abscess. 

In cases presenting the characteristic features of brain abscess, the 
sudden development of very severe and persistent headache would render 
the prognosis more grave in pointing to probable extension of the disease 
to the meninges. 

To whatever lesion the headache may be due, the part of the head to 
which the pain is referred furnishes no reliable indication of the site of the 
lesion; for either in cerebral or cerebellar abscess or in meningitis, the pain 
may be referred either to the frontal or to the occipital region, or less 
frequently to the vertex, or it may migrate from one to the other. 

Vomiting. —Aside from that due to digestive disorders, vomiting may 
be induced reflexly by so many peripheral disorders that one should be in 
no haste to refer its origin to a supposed lesion within the skull. Neverthe¬ 
less, it is an accepted fact that the act of vomiting is under the control of a 
“ centre,” possibly in the medulla, and excited through the medium of the 
vagus; and it is a reasonable hypothesis that this centre may be irritated, 
either directly or through association fibres, by various intracranial lesions. 

Starr says that vomiting may be induced by apoplexy (initial stage), 
by brain tumor or abscess, or by meningitis. Gowers states that “organic 
disease in any part of the brain may cause vomiting.” According to Mac- 
ewen, “vomiting occurs in the initial stage of brain abscess,” but rarely 
after the abscess is fully formed. Vomiting, then, may be caused by any 
lesion so situated as to irritate or press upon certain nerve centres at the 
base of the brain. 

In its most typical form, central vomiting presents the following 
characteristics: It is projectile, is not accompanied by nausea or the usual 
signs of disturbed digestion, and is not influenced by remedies usually 
corrective of gastric disorder. While this describes the type, it is not safe 
to assume that vomiting is not of central origin simply because symptoms 
of digestive disturbance are present. The central irritation may be suffi- 


324 


SYMPTOMS OF INTRACRANIAL DISEASE 


ciently pronounced to induce independent contraction of the stomach with 
projection ol its contents, or may fall short of this result, leaving the ner¬ 
vous control mechanism of the stomach in a state of irritable unbalance 
easily, acted upon by slight peripheral causes. 

Vomiting, with or without nausea, occurs so much more frequently 
with meningitis than with other intracranial lesions that, taken alone, it 
must be regarded as pointing rather strongly to meningeal disease. 

Next to meningitis there can be no doubt that vomiting is more fre¬ 
quently present with cerebellar abscess than with any other brain lesion. 
While it rarely occurs after the onset, or formative stage, of cerebral abscess 
(Macewen), the author has observed several cases of cerebellar abscess 
in which it was a rather prominent symptom not only at the onset but 
recurred at intervals throughout the entire course of the disease. 

Aside from its frequent association with meningitis, vomiting is a 
general rather than a focal symptom. In association with other symptoms, 
however, it may be of considerable value in determining the site or charac¬ 
ter of an intracranial lesion. Among such combinations may be mentioned 
the following: 

1. Recurrent vomiting with nausea, accompanied by rotary nystag¬ 
mus, vertigo, and ataxia, showing rapid and progressive diminution in 
severity, suggests suppurative labyrinthitis. 

2. Recurrent vomiting without nausea, accompanied by rotary nys¬ 
tagmus, vertigo, and ataxia, persistent or tending to increased severity, 
strong^ suggests cerebellar abscess. 

3. Recurrent vomiting with incoordination ataxia of one or both hands, 
high temperature and tendency to delirium being persistently absent, 
suggests cerebellar abscess. 

4. Recurrent vomiting with headache, fever, and tendency to delirium 
points almost with certainty to meningitis. 

Gowers’s Syndrome .—Gowers believes that persistent headache coupled 
with persistent vomiting, for which no discernible cause is present, and 
which is not relieved by any of the usual remedies, constitutes an important 
syndrome which in itself is very strongly diagnostic of intracranial disease. 

Temperature Changes. —Moderate temperature variation may be 
excited by causes too various for it to be of great diagnostic value except 
in association with other symptoms. There are, however, certain facts 
which may well be borne in mind in examining the temperature chart in a 
case of suspected brain disease. It is probable that most suppurative 
brain lesions are ushered in by a rise of temperature. If, however, it be 
situated well beneath the cortex in the cerebral substance,— e.g. } a cerebral 
abscess,—the temperature after the lesion is fully developed may return 
to normal and remain so for considerable periods. In deep-seated cerebral 
lesions, therefore, the temperature may furnish absolutely no evidence of 
the actual condition. On the other hand, any form of inflammation in¬ 
volving the meninges or the cerebral cortex is commonly announced by an 
elevation of temperature which, though varying in degree, is usually more 


TEMPERATURE AND PULSE CHANGES 


325 


or less continuous. A continuously normal temperature is usually suffi¬ 
cient, therefore, to exclude meningeal involvement; and, per contra, in 
suspected intracranial disease constant elevation of temperature is rather 
strongly suggestive of a cortical lesion,— i.e., meningitis or peripheral 
encephalitis. 

The only intracranial disease to which, after exclusion of other causes, 
the temperature may furnish the positive clue is infective sinus thrombo¬ 
sis. Naturally an infected clot, situated within a large venous channel, 
and from which infected particles may be periodically discharged directly 
into the general circulation, might be expected to give rise to a very charac¬ 
teristic type of temperature variation,—the intermittent type character¬ 
istic of periodic septic absorption. 

Changes in Pulse-rate. —Within certain limits the pulse-rate varies 
in acute intracranial disease in accordance with the same laws which 
regulate its changes in acute disease originating in other parts of the body. 
That is to say, it is probable that the temperature is elevated and the pulse 
quickened at the onset of every acute suppurative lesion involving either 
brain or meninges. It is also an established clinical fact that in nearly 
every fatal case of acute intracranial disease the pulse is greatly accele¬ 
rated shortly before the end. Between the initial and terminal stages, how¬ 
ever, the pulse-rate may show changes of the greatest diagnostic importance. 

It has been noted in many cases of brain abscess that the pulse-rate 
at some stage of the disease has been markedly reduced in frequency. 
This occurs quite as often with abscesses of the cerebrum as with those of 
the cerebellum. The same lowering of the pulse-rate has been frequently 
observed also in connection with rapidly growing brain tumors. It has 
also been noted in certain cases of purulent leptomeningitis. The phe¬ 
nomenon seems, therefore, to be due largely, but not always solely, to 
increased intracranial pressure. 

The relation between reduced pulse-rate and such lesions has frequently 
been demonstrated by post-mortem findings and by surgical intervention. 
Furthermore, in many cases of brain abscess, the slow pulse-rate has been 
immediately corrected by surgical evacuation of the pus (Macewen). 
When, therefore, a patient suffering from suppurative middle-ear or mas¬ 
toid disease suddenly exhibits a markedly reduced pulse-rate,— e.g., 60, 
50, or 40 beats per minute,—this symptom alone is rightly regarded as 
rather strongly suggestive of brain abscess. 

Somewhat puzzling are certain cases of meningitis in which a reduced 
pulse-rate has been observed. While increased intracranial pressure is, 
of course, common in some forms of meningitis, it seems probable that 
there may be other causative factors at work in the bradycardia of such 
cases,— e.g., an accompanying encephalitis causing perhaps irritation or 
excitation of some centre exerting an inhibitory influence over the heart¬ 
beats. This is apparently the view held by Gowers. Such cases, however, 
are somewhat exceptional. As a rule, all forms of meningitis are accom¬ 
panied by an acceleration of the pulse-rate. 


32 6 


SYMPTOMS OF INTRACRANIAL DISEASE 


The slow pulse resulting from the formation of a brain abscess is usually 
a changing symptom, having some relation to the increasing pressure. 
The reduction of the pulse-rate is not, however, in direct proportion to 
the size of the abscess,—a very small abscess sometimes causing very 
appreciable slowing of the pulse. If the abscess becomes encapsulated,— 
i.e., enters upon a latent stage of indefinite duration,—it is probable that 
the intracranial pressure undergoes gradual readjustment with restora¬ 
tion of the normal pulse frequency. On the other hand, rupture of a brain 
abscess with escape of pus either into the ventricles or subarachnoid space, 
is invariably announced by a train of alarming symptoms, among which 
an exceedingly rapid pulse is always prominent. 

Macewen’s Syndrome .—Macewen has called attention to the combina¬ 
tion of two symptoms,—viz., high temperature associated with subnormal 
pulse-rate,—as strongly diagnostic of intracranial disease. The author 
believes that this association—even when the fever is not high and the 
pulse retardation is of moderate degree—is most important. It is so diffi¬ 
cult to think of any lesion outside of the skull cavity which could give rise 
to this phenomenon, that he is inclined to regard it as pathognomonic, 
not of any particular lesion, but of intracranial disease. 

Unilateral Muscular Spasm as a Symptom of Cerebral Disease. 
—General convulsions— i.e., of both sides of the body—rarely occur as the 
result of a cerebral lesion of otitic origin. On the other hand, unilateral 
spasms confined to certain groups of muscles may point quite clearly to 
irritation by such a lesion of the motor centres of the muscles involved. 
The condition may consist merely of twitching of a single muscle or muscle 
group, or may be so severe as to justify the term localized convulsion, which 
condition is known as Jacksonian epilepsy, after the man who first described 
it. 1 In a typical case the symptoms occur somewhat in the following order: 
First a sensation of tingling in the limb or region involved, then there is an 
involuntary contraction of a single muscle or muscle group, this being fol¬ 
lowed by clonic spasms or convulsions, other related muscle groups being 
successively involved. Thus, the contractions may begin at the shoulder 
and gradually extend down the arm so as to include the wrist and fingers, or 
they may commence in the fingers and extend in the opposite direction tow¬ 
ard the shoulder. In either case the spasms of these muscles would point 
to irritation of the middle third of the precentral or ascending frontal gyrus. 
Or the convulsion may in a similar way involve the muscles of the lower 
limb, which would point to irritation of the paracentral or upper third of 

1 Hughlings Jackson, of London, published in 1861 the first recorded series of cases 
in which the patients, having suffered from a peculiar form of unilateral spasm confined 
to certain muscle groups (“Jacksonian epilepsy”), were subjected post mortem to care¬ 
ful examination in the dead-house. The post-mortems showed uniformly lesions involv¬ 
ing certain cortical areas of the opposite cerebral hemisphere, which he therefore assumed 
to be the motor centres of the muscles in which contractions had occurred. These 
records provided the starting-point and foundation upon which our knowledge of cere¬ 
bral motor localization has been built up. 




MUSCULAR SPASMS; PARALYSIS 


327 


the precentral convolution. Another typical Jacksonian attack is charac¬ 
terized by convulsive lateral movements of the head and eyes to one or 
the other side ,—i e., there are coincident lateral nystagmus and successive 
jerky movements of the head in the horizontal plane in one direction until 
the face looks over one or the other shoulder. This phenomenon is caused 
by irritation of the motor centre for the head and eyes, which is located in 
the posterior end of the second or middle frontal convolution. The move¬ 
ments are toward the shoulder opposite to the side of the lesion. In these 
attacks there is no loss of consciousness. The convulsion may last several 
minutes, and, in accordance with its severity and duration, leaves the mus¬ 
cles in a condition of flaccid weakness or actual paralysis, which, however, 
is only temporary. If such an attack has been carefully observed, much 
may be learned from the order in which it occurs. Thus, the premonitory 
tingling, which may precede the convulsion by several minutes, is usually 
referred to the region of the initial contraction; and the initial contraction 
will throw light on the initial centre of irritation in the cerebral cortex. 
The subsequent muscular paralysis, or weakness, will be most marked in 
the muscle group in which the spasms first occurred, and these muscles 

will be the last to recover their tone and power. 

It is generally conceded that a cerebral lesion can cause muscular 
spasms only when so placed as to be capable of causing, either diiectly oi 
indirectlv, irritation of the cortical motor area. lor this reason many cases 
of intracranial disease end fatally, or are relieved by surgical intervention, 
without ever having produced motor disturbances of any kind. Never¬ 
theless, it is known that a cortical lesion primarily outside of the Rolandic 
area may by cortical extension involve the motor area, and it is clear that 
a subcortical lesion may by peripheral extension also involve the cortex. 
It seems evident that irritation from a subcortical lesion, acting by pres¬ 
sure or through its proximity to the cortex, would give rise to but slight 
muscular contractions as compared with an irritative lesion of the cortex 
itself. Nevertheless, such slighter phenomena might throw much light 
upon an otherwise obscure lesion. The symptoms should therefore be 
borne in mind in every case of suspected intracranial disease of otitic 
origin. When localized muscular spasms do occur in the course of a brain 
lesion, they point clearly to the following facts,—viz.: (a) that the lesion, 
if subcortical, is sufficiently peripheral to cause cortical irritation; (b) that, 
if cortical, it must be so situated as to involve either directly or by lateral 
extension the precentral, or motor, area; and (c) if the sequences of the 
attack have been carefully observed, they may supply further data as to 

its exact localization. 

Unilateral Muscular Paralysis or Paresis.— The results of cor¬ 
tical lesions in the motor area of the brain are so generally understood as 
hardly to require more than passing mention here. Destructive lesions 
in any part of the motor area of either cerebral hemisphere are followed 
regularly by volitional paralysis, partial or complete, of the corresponding 
muscle-groups of the opposite side of the body. r I hus, a paralysis of cere- 


328 


SYMPTOMS OF INTKACKANIAL DISEASE 


bral origin confined to the wrist or elbow muscles of either side would 
suggest a cortical lesion of the middle third of the ascending frontal con¬ 
volution of the opposite cerebral hemisphere; while paralysis of the foot or 
leg muscles would point to a lesion in the upper third of the same convolu¬ 
tion. But paralysis of the same muscle-groups may also result from any 
subcortical lesion within the motor tract, which includes the projectional 
fibres of the appropriate cortical centres. A brief reference, therefore, to 
the common paralytic effects of such subcortical lesions, as compared with 
those usually resulting from a cortical lesion of equal size, may be permis¬ 
sible here. 

From the under surface of the motor (precentral) area, the projectional 
fibres converge to meet in the internal capsule and there form the densely 
arranged motor tract which from this point is continued downward through 
the crus cerebri, pons varolii, and medulla to the opposite side of the cord. 
It is obvious that, in their passage from the cortex to the internal capsule, 
the fibres from the lower third of the precentral, or ascending frontal, 
convolution pass more or less horizontally inward, while the fibres of the 
middle third must assume more oblique directions gradually approaching 
the vertical plane. Finally the motor fibres of the upper third pass down¬ 
ward and somewhat outward around the lateral ventricle to join those of 
the lower and middle thirds in the internal capsule. This arrangement is 
shown in the diagrammatic figure (Fig. 186), which also shows very graph¬ 
ically the varying results of lesions in the cortex and in the motor tract. 
The darkened areas represent destructive lesions in the cortex, internal 
capsule, and crus cerebri. Numbers 1, 2, and 3 represent cortical lesions 
in the motor areas of the leg, arm, and face respectively. It is obvious 
that an} r one of these, occurring singly, could give rise to paralysis of but 
one set of muscles,— i.e., those of the leg, arm, or face; and that similar 
monoplegias might result from subcortical lesions in the centrum ovale 
involving the projectional fibres from single motor centres (4 and 5). If, 
however, we follow these projectional fibres from the various motor centres 
into the internal capsule, it becomes clear that a comparatively small 
lesion in this situation (6) would be likely to result in more widespread 
paralysis (hemiplegia). 

While it is perhaps theoretically possible for a small lesion situated 
in the internal capsule to involve the projectional fibres of one motor 
centre only, with consequent monoplegia, this is exceedingly unlikely to 
occur. A comparison of the autopsy finding with the clinical records in 
fatal cases of paralysis due to cerebral lesions would seem to show that in 
the great majority of cases, lesions of the internal capsule, if sufficiently 
severe to intercept motor impulses, give rise to rather widespread paralysis; 
and conversely, that a majority of all cases of hemiplegia resulting from 
suppurative brain lesions are due to lesions involving the internal capsule. 
On the other hand, only the most extensive cortical lesion could give rise 
to widespread paralysis. While an abscess confined to the temporosphe- 
noidal lobe the usual seat of an otitic abscess—might through transmitted 


MUSCULAR PARALYSIS 


329 


pressure give rise to extensive paresis, complete hemiplegia— i.e., involving 
equally upper and lower limbs—is rarely or never so produced. As in the 
internal capsule, so in the crus cerebri, pons and medulla oblongata, lesions 
of the motor tract give rise to paralysis coextensive with the cortical area 
whose motor fibres are interrupted. 

From the fact that the motor oculi nerve arises from the inner side of 
the crus cerebri and supplies the ocular muscles on the same side as the 
crus from which it springs, a lesion in this situation (7) is apt to produce a 



Fig. 186.—Diagrammatic picture of a transverse section of the brain. (Modified from Starr.) 

characteristic form of paralysis, i.c., to involve the motoi tract supply¬ 
ing the muscles of the opposite side of the body (hemiplegia), and the 
third nerve (ocular paralysis) on the same side as the lesion. 

So far as we may formulate deductions from the above, they may be 

stated as follows: ... . 

(a) In suppurative intracranial disease, however originating, paraly sis 

of a single group of muscles suggests a cortical lesion, oi a lesion so placed 
in the centrum ovale as to intercept only the projectional fibres of the motor 

centre involved. 

(b) Hemiplegia, or widespread unilateral paralysis, points with greater 
probability to a lesion involving the internal capsule. 

(c) Unilateral ptosis with external squint and inability to rotate the 





















330 


SYMPTOMS OF INTRACRANIAL DISEASE 


eyeball upward, inward, and downward, accompanied by paralysis of the 
leg, arm, and face muscles of the opposite side, points to a lesion of the 
crus cerebri on the side corresponding to the ocular symptoms. 

Mental Disturbances. —The relation of mental disturbances to intra¬ 
cranial disease is hardly within the scope of a manual of otology. The 
author wishes merely to refer briefly to certain forms of mental disorder as 
having a practical bearing upon the diagnosis and prognosis of brain 
lesions of otitic origin. So far as he has been able to observe, the mental 
symptoms occasionally characterizing these lesions conform almost inva¬ 
riably to one or other of three main types,—viz.: (1) Depressed or retarded 
cerebration, due usually to a lesion producing great increase in intracranial 
pressure; (2) loss of cerebral control , leading first to mental excitement and 
finally to delirium, due usually to an irritative lesion of the cortex or the 
meninges; and (3) apraxia, or inability to think coherently, this being due 
to a loss of the concepts of familiar things. 

1. Depressed or Retarded Cerebration .—In this condition cerebration 
may be obscured almost to the point of cessation. It is a condition of 
extreme mental lethargy. As a consequence, there is more or less difficulty 
in commanding the patient’s attention even to simple questions. Having 
gained his attention, he answers, if at all, correctly. Sometimes there is 
distinct evidence of retardation of the mental process. Having asked him 
a question and waited for a reply, the answer comes after a long delay, 
just when you have concluded that he has either not heard or not under¬ 
stood. The condition is frequently accompanied b}^ a tendency to lethargic 
somnolence. He may ask for something, and doze off, forgetting his 
request, before it can be brought. Evidently, the mental processes are 
obscured, retarded, minimized, but neither ablated nor perverted. 

This form of mental disturbance is usually the result of great increase 
in intracranial pressure, as in the case of a large and rapidly formed brain 
abscess. It is not of itself an evil prognostic sign, since it usually charac¬ 
terizes a lesion which may respond favorably to surgical treatment,— 
e.g., the successful evacuation of a brain abscess. 

2. Delirium may be of low, mattering form or of the violent type, in 
which the patient screams, uses wild or abusive language, and can with 
difficulty be kept in bed. In either case the condition is equivalent to 
mental oblivion, since the patient, if he regains his mental balance, never 
has any knowledge or memory of what has occurred. 

Delirium resulting from intracranial infection usually points to a cor¬ 
tical lesion,— i.e., peripheral encephalitis or meningitis. It is of unfavor¬ 
able prognostic significance, in that it points to a type of lesion which ends 
oftener in death than in recovery. 

3. Apraxia describes a condition in which the patient, though con¬ 
scious and perhaps striving to think coherently, is unable to do so because 
he can not command clear and complete mental pictures of familiar objects. 
It is demonstrated when a person by the incoherence of his speech shows 
that he is unable to recognize or appreciate the nature or uses of things 


APHASIA 


331 


about him. Etiologically it bears a strong analogy to the various forms of 
aphasia (next to be described), with some of which it coexists. In right- 
handed individuals it indicates a lesion in the left cerebral hemisphere 
and vice versa. It is not necessarily an unfavorable prognostic sign, pro¬ 
vided the site and character of the lesion can be determined. 

APHASIA. 

The subject of aphasia is so large, and its causes so deeply rooted in 
neurology, that we can attempt here only a brief description of such speech 
defects as may occasionally occur in brain lesions of otitic origin. 

By aphasia we mean loss of the power of expressing one’s thoughts 
intelligibly in spoken words. This definition is elastic, as it should be, 
for the aphasic individual may be practically or nearly speechless (motor 
aphasia); or his words may come in disordered and meaningless sequence 
(paraphasia); or he may be unable to recall a familiar object from the sound 
of its name, and, since all name-sounds have ceased to have any mental 
associations, he is also unable to command the name of a familiar object 
seen (word-deafness). Any of these defects may result from a cerebral 
abscess of otitic origin. 

Inability to convey one’s thoughts correctly in spoken words is not 
infrequently associated with inability to recognize written words or sym¬ 
bols (word-blindness), in which case the individual would naturally be 
unable to write at will,—or, rather, to express his thoughts in writing 
(agraphia). 

Again, either aphasia or agraphia may be of two main types.— i.e ., 
either sensory or motor. 

The cortical centres, the integrity of which is essential to intelligible 
speech, are in the left side of the brain in right-handed persons, and vice versa. 

Before attempting to trace these commoner forms of aphasia to their 
appropriate lesions, it may be well to recall briefly the physiological basis 
of coordinate speech. It will be remembered that, as with the convolutions 
of the brain, so the smallest cortical “centres” are brought into relation 
with each other and with other parts of the cerebrospinal system by three 
sets of fibres,—viz., (a) association fibres which pass from one centre to 
another, and by virtue of which the smallest cortical area is said in some 
degree to be associated with every other; (b) commissural fibres which pass, 
as in the corpus callosum and anterior commissure, from one hemisphere 
to the other, and by virtue of which the two hemispheres act as one organ; 
and (c) the projectional fibres which pass from each cortical centre to the 
base of the brain and spinal cord. 

The time intervening between a baby’s birth and its first efforts at 
intelligible speech is consumed not so much in acquiring the physical 
power of articulation, as in storing the mind with certain impiessions, or 
11 memory pictures,’’ which are essential to coordinated thought, this 
being prerequisite for coordinated speech. I he lowest type of idiot can 
not acquire language because coordinated thought is to him impossible. 


332 


SYMPTOMS OF INTRACRANIAL DISEASE 


“The basis of language/’ Starr tells us, “is a series of memory pictures/’ 
and these memory pictures are stored in various special centres for the 

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reception and retention of such impressions. Thus, before the child can 
make intelligent use of the simplest noun, he or she must have a series of 
memory pictures relating to it stored in various memory centres in differ- 












THE APHASIC CENTRES 


333 


ent parts of the cerebral cortex. Taking, for example, the word “doll,” 
the child must have, first, a definite memory picture of the sound of this 
word, and this is stored in a special cortical centre for the memory of 
various sounds. This centre is located in the middle of the first and second 
temporal convolutions (Fig. 187, a). Next, she must have also a definite 
memory picture of the shape, general color scheme, and common sizes of 
dolls,— i.e., a visual impression based upon the dolls she has seen. The 
special memory centre for visual impressions of various objects is located 
in the second occipital convolution (Fig. 187, b). And, third, she must 
have a definite impression of the texture or solidity of the various parts of 
the doll, this memory picture being stored in a special area for the reten¬ 
tion of tactile impressions of various objects. This centre probably in¬ 
cludes adjacent portions of the posterior central and superior and inferior 
parietal convolutions (Fig. 187, c). To these memory pictures—^.e., of 
the sound of the name, the visual impression of the image, and the tactile 
impression of its texture and consistency—must be added a memory picture 
of the motor effort required to produce the articulate sound, this being 
stored in a special centre located in Broca’s convolution (Fig. 187, d). It 
is now quite intelligible that these four memory impressions, brought into 
relation and coordinated through the association fibres passing between 
the various memory centres involved, should produce a concept, or complex 
mental image, and that this concept is essential to the intelligent use of 
the word. It is also a logical deduction that destruction by injury or 
disease of any of these memory centres, or of the association fibres through 
which their impressions are combined and coordinated, might easily pro¬ 
duce defects of speech,— i.e., some form of aphasia. 

It is clear that in addition to the four “memory pictures” above de¬ 
scribed, and which probably constitute the essentials of the earliest and 
simplest conception of the child’s mind, there are also innumerable other 
memory impressions relating to the object named, i.e., its uses, advant¬ 
ages and disadvantages of certain kinds, its associations by analogy or 
contrast with similar or dissimilar objects, etc., which come with in¬ 
creasing experience and advancing mental development. With the edu¬ 
cated adult, for example, the concept of each object must include at least 
two additional centres for the special memory pictures which enable him 
to read and to write, respectively:— i.e., he must have memory pictures of 
the appearance of written words and letters, the special centre for such 
impressions being located in the angular gyrus (Fig. 187, e) ’, and he must 
have a memorj^ picture of the motor acts required to form the letters and 
particular words. Destruction of the first of these i.e., the visual word 
centre—would render the individual unable to read. Destruction of the 
centre for the motor or effort memories of writing would render him unable 
to write, though he might still be able to read with understanding. 

Obviously, with normal individuals the special senses—particularly of 
hearing, sight, and touch—are essential factors in the development of overly 
complete concept. The cortical centres for the special senses of sight, 


334 


SYMPTOMS OF INTRACRANIAL DISEASE 


hearing, touch, etc., therefore play an essential part in the normal auto¬ 
matic development of speech. The congenitally blind are slow in learning 
to talk. The child absolutely deaf from birth never acquires language 
except through artificial methods of instruction. 

With the above facts in mind, the various speech defects become more 
intelligible to us; for it is clear that we can interfere with the processes of 
coordinated thought and speech either by destruction or injury of one or 
more of the special memory centres involved, or by destroying the associa¬ 
tion fibres by which they are connected. We are now better equipped to 
study the different forms of aphasia as aids to diagnosis. 

Suppose, for example, that we are examining a right-handed individual 
suspected of having an abscess in the left cerebral hemisphere. We begin 
by asking him very simple questions requiring chiefly affirmation or nega¬ 
tion,— e.g.j if he feels any pain; if he is married; if he has children, etc., 
etc., receiving intelligent replies which indicate that up to a certain point 
his cerebration is normal. 

Sensory Aphasia. — Partial Word-deafness. —We now show him some 
familiar object, as, for example, a penknife, and ask him to name it. He 
can not do so, and may call it a “key” or a “pencil.” Ask him what it is 
used for, and he answers correctly,— e.g., “to cut with.” Ask him if it is a 
key, a pencil, or a penknife, and he corrects his former statement and says 
that it is a penknife. Now ask him the uses of articles not exposed to his 
view,— e.g., “what is a pencil used for?” “What is a watch used for?” etc. 
He may be unable to answer correctly. This condition is one of sensory 
aphasia due to 'partial word-deafness, —partial because, though unable to 
name a familiar object shown him, he can, when several names are spoken 
for him, select the correct one. Though he may be unable to recall the 
uses of an object from the sound of its name alone, he can, if both the name 
be sounded and the object shown him, recall their relation. In other words, 
both the auditory and the visual memory pictures are intact, but there is 
a break in their association through a lesion involving the association 
fibres by which the auditory memory centre is brought into relation with 
others. In such a case, the lesion is subcortical and one which has to a 
great extent cut off the special centre for sound memories from its associa¬ 
tion with the other memory centres essential to intelligent speech. One 
would expect in such a case a subcortical lesion in the neighborhood of the 
first and second temporal convolutions. This, in the writer’s experience, 
is the commonest form of aphasia in cases of brain abscess of otitic origin. 

Total Word-deafness. —If the patient is unable to call the name of a 
familiar object shown him, though recognizing its character and uses, 
and, when its name with several others is spoken for him, is still unable to 
call the correct one, the condition is one of total word-deafness and presum¬ 
ably due to a cortical lesion involving the special centre for sound memories. 
Such a lesion usually produces great confusion of speech, and also renders 
his mother tongue almost incomprehensible to him. It is exceedingly 
rare as a result of suppurative brain lesions. 


APHASIA 


335 


Inter cortical Motor Aphasia. —This condition is produced by a sub¬ 
cortical lesion which injures, or presses directly upon, the association fibres 
connecting Broca’s convolutions (motor speech memories) with the other 
memory centres. The other memory centres essential to coordinated 
thought being intact, and their interassociation not disturbed, the patient’s 
cerebration is not necessarily disturbed. He understands what is said to 
him, and can express his thoughts in writing. He therefore makes con¬ 
scious and strenuous efforts to express himself coherently in speech, but 
without success, the words and even syllables being transposed, and fol¬ 
lowing each other without intelligible sequence. According to Starr, this 
variety of speech defect is produced by lesions involving the association 
tract between Broca’s centre and the temporal auditory memory area, 
which tract passes beneath the island of Reil. 

Word-blindness (causing Sensory Agraphia). —The special centre in 
which are stored visual memory pictures of objects seen and visual centre 
for written symbols,— i.e., written or printed letters, words, etc.,—are not 
identical,—the former being located in the second occipital convolution, 
and the latter in the angular gyrus (Fig. 187, e). 

It is possible that an individual with a brain lesion— e.g., abscess— 
may be able to answer all questions intelligently, and to recognize the 
character and uses of any familiar object shown him and to give its name 
correctly, yet may be quite unable to read a single word of written or 
printed matter. He may be unable to recognize even the letters of the 
alphabet. This condition is called word-blindness (alexia), and is caused 
by a subcortical lesion which cuts off the centre for the memory pictures of 
written symbols from the other memory centres essential to coordinated 
speech. And, since the patient can not recall the form and appearance of 
the letters and written words, he is also unable to write. He may, however, 
be able to copy written matter, but does so with little or no understanding 
of the sense, or meaning, conveyed. This form of agraphia is called sensory, 
in contradistinction from the condition in which the patient recalls the 
forms of letters and written words, and can therefore read understanding^, 
but is quite unable to inaugurate the finger movements necessary in writ¬ 
ing (motor agraphia). 

Word-blindness and consequent sensory agraphia are determined by 
testing the patient’s ability to read and write simple sentences in his 
mother tongue. The condition may occur independently or coexist with 
word-deafness. 

Sensory Visual Aphasia (Psychical Blindness). —Again, if we suppose 
or find that our patient is unable either to name a familiar object shown 
him or to bring to mind its uses, but that he can recall its name when this, 
with others, is spoken for him, and from its sound can also recall its uses,—• 
we have another variety of sensory aphasia dependent upon what is some¬ 
times called psychical blindness. It is due to a subcortical lesion which 
practically isolates the special memory centre for visual impressions of 
objects seen. The “centre” is not actually destroyed, for the visual 


336 


SYMPTOMS OF INTRACRANIAL DISEASE 


memory pictures can be recalled by the sound of the name acting through 
certain indirect associational tracts. In such a case, we should not be 
surprised at finding the lesion rather far back,— i.e ., in the region of the 
second occipital convolution. 

Motor Aphasia.—A somewhat kindred lesion, but producing quite 
different functional defects, is known as motor aphasia. This is due to a 
lesion directly involving the centre in which are stored the motor effort- 
memories necessary to the production of articulated speech (Broca’s 
centre,—posterior part of third frontal gyrus). The patient can not talk, 
can not even repeat sentences word for word after another. He may, 
however, retain the use of a few monosyllabic words,— e.g., yes, no, etc. 
This incapacity for speech may coincide with intelligent understanding 
of what is said,—this apparent anomaly being indicated by his gestures in 
response to questions, and possibly in some cases by the ability to convey 
his meaning in writing. 

Motor agraphia, occurring alone,— i.e., without disturbances of co¬ 
ordinated thought or speech,—is probably an exceedingly rare condition. 
For a typical case, we would have to suppose a lesion, cortical or sub¬ 
cortical, which had involved directly and solely, or at least cut off from 
association with other memory centres, the special centre for the motor 
effort-memories essential to the act of writing. The patient, while able 
to read printed or written matter with understanding, and while showing 
no evidences of apraxia, 2 is unable to write a single word. He can neither 
express his thoughts in writing, write at dictation, nor even copy the sim¬ 
plest sentence. 

Motor agraphia and motor aphasia not infrequently coexist,—the 
effort-memory centre for writing being supposed to be not distant from 
the centre in which are stored the motor speech memories. 

The differential points between motor agraphia (without motor apha¬ 
sia) and sensory agraphia are repeated below: 


Motor Agraphia. 


Sensory Agraphia. 


Due to a lesion which inhibits solely 
the mechanical act of writing; patient can 
therefore read with understanding. 


Sensory agraphia is part of the con¬ 
dition known as word-blindness; patient 
cannot therefore either read or write. 


Patient cannot write either at will or 
from a copy. 


Patient cannot write at will, but usu 
ally can write from copy. 


2 Apraxia is a term used to describe the inability to think coherently which results 
from a loss of the concepts of familiar things. 



CHAPTER XIII. 


INTRACRANIAL LESIONS OF OTITIC ORIGIN: EXTRADURAL 

abscess; perisinous abscess; septic sinus thrombosis 
or phlebitis; purulent leptomeningitis; cerebral 
abscess; cerebellar abscess. 

Avenues of Infection (Fig. 188).—Aside from the more favorable 
avenues of escape through the external cortex, it is clear that pus within 
the mastoid may travel in various directions, and in accordance with its 



Fig. 188.—(Diagrammatic.) Otitic pathways of pus to brain or meninges, (a) Epidural abscesses; 
(f>) temporosphenoidal abscess; (c) perisinous abscess; (d) sigmoid sinus thrombosis; (e) site of epi¬ 
dural abscess in contact with cerebellum; (/) convenient space for exposing cerebellar dura and which 
may represent nearest point for opening cerebellar abscess, pus travelling from (e), (y) infection of 
jugular bulb, pus travelling downward from tympanum, or downward and forward from mastoid cells, 
or reaching bulb by the most usual route,— i.e., from an infective lesion (d) in sigmoid sinus. 


point of entrance may lead quite logically to different lesions within the 
cranium. Thus, it may perforate the roof, or tegmen antri, giving rise 
to an extradural abscess (a); or, as a later development of this lesion, to a 
cerebral abscess (b); or it may travel backward toward the posterior fossa 
of the skull, causing either a perisinous abscess (c), infective sigmoid 
sinus thrombosis or phlebitis (d); an extradural abscess in the neighbor¬ 
hood of the cerebellum (e), or a cerebellar abscess (f). Passing downward 
and forward from the mastoid, or downward from the tympanic cavity, the 
infection may spread directly to the jugular bulb (g), giving rise to a septic 
lesion within the jugular vein, not clinically distinguishable from a sup¬ 
purative lesion within the lateral or sigmoid sinus. 

It is obvious that germs entering the cranial cavity by any of the path- 


































338 


INTRACRANIAL LESIONS OF OTITIC ORIGIN 


ways above indicated may directly attack the meninges, giving rise either 
to a limited pachymeningitis or to a circumscribed or widespread purulent 
leptomeningitis. Fortunately, the latter condition is comparatively rare 
as a result of infection reaching the cranium by these routes, except as 
a complication of some suppurative lesion of the brain. 

Still another very important pathway is furnished by the intermediate 
infection of the labyrinth. Pus from the infected labyrinth may reach 
the cranial cavity by three routes,—viz., (1) through the nerve channels 
into the internal auditory meatus, (2) from the cochlea through the aqusc- 
ductus cochleae, or (3) from the vestibule through the aquieductus vestibuli. 
Pus entering the cranium by any of these routes is particularly prone to 
cause widespread purulent leptomeningitis. Less frequently it causes 
cerebellar abscess or sigmoid sinus thrombosis. It must not be forgotten 
that pus reaching the cranium through the aquaeductus cochleae passes 
directly into the subarachnoid space. 

EXTRADURAL ABSCESS,* EPIDURAL ABSCESS. 

The term extradural, or epidural, abscess is applied to any circum¬ 
scribed collection of pus between the dural covering of the brain and the 
contiguous bone surface. It is the commonest of intracranial lesions of 
otitic origin. While not per se a dangerous condition, it is not without 
grave possibilities in the brain lesions to which it may give rise. Bezold 
believed that the presence of pus between dura and bone is a preliminary 
or intermediate stage of nearly every case of brain abscess. 

Etiology. —The causes may be deduced from what has been said as 
to the possible avenues of infection. Great virulence of infection in a 
mastoid of pneumatic type, and in which the plates separating the mastoid 
and cranial cavities are thin, would seem to provide a favorable condition 
for the formation of these secondary collections of pus. On the other hand, 
a thick cortex, small pneumatic spaces, and pus under pressure would 
seem equally to favor their development. While depressed constitutional 
states should theoretically influence the rapid extension of bone necrosis, 
it has not been observed that old people or patients whose vitality is con¬ 
siderably below par develop this simplest complication of mastoid sup¬ 
puration any oftener than the young or physically robust. 

Extradural abscess occurs with far greater frequency in acute mas¬ 
toiditis than with chronic suppurative otitis media with mastoid involve¬ 
ment. The lesion does occur, however, as a result of chronic middle-ear 
and mastoid suppuration. The discovery during the radical operation of 
an area of exposed dura is not particularly rare, and it is quite possible 
that this condition may represent in some cases an earlier collection of 
pus beneath the bone. 

Symptoms. —The symptoms of epidural abscess may be nil or so indefi¬ 
nite as to be of little or no diagnostic value. The usual absence of charac¬ 
teristic symptoms, or our inability to interpret them correctly, is indicated 
by the fact that the lesion is rarely diagnosticated prior to operation for 
the relief of acute mastoiditis. 


EXTRADURAL ABSCESS; EPIDURAL ABSCESS 


339 


Among the symptoms which may be present are (a) severe localized 
pain, (b) severe headache, generalized or confined to the side of the lesion, 
and (c) elevation of temperature. These symptoms may, however, be 
wholly wanting, and, when present, their value is minimized by the fact 
that one or any of them may be present in severe uncomplicated mastoi¬ 
ditis. While it is an established fact that large extradural collections of 
pus occasionally give rise to focal or general symptoms of intracranial 
pressure, such symptoms are comparatively rare as a result of this lesion. 

As physical signs we have sensitiveness to pressure over the site of the 
abscess—usually above the mastoid—and sensitiveness to light percussion 
over the mastoid region. These also are inconstant. The diagnosis is, 
therefore, usually dependent upon accidental opening of the abscess, or 
intentional exploratory uncovering of the dura on account of unusual 
severity of symptoms. Or, again, exposure of the dura may be made 
necessary by physical evidences of necrosis in the inner plate. 

Extradural abscesses vary considerably in size, amounting in some cases 
to but a few drops of pus bathing the dural surface, in others reaching a 
very considerable amount confined under some pressure. In the case of 
large pus collections localized by surrounding adhesions between bone and 
dura, it is evident that the latter may be subjected to abnormal strain and 
tension. It is probably the latter condition which is chiefly responsible for 
the pain in certain cases. 

Another physical variation which these cases exhibit is in the condition 
of the dura, which may be quite normal in appearance or may be covered 
with granulations,—this representing one stage of a localized pachymen¬ 
ingitis. Even in the presence of this latter condition, the symptoms are 
usually not sufficiently definite to form the basis of a diagnosis prior to 
operation. 

The most common site of an otitic epidural abscess is between the 
tegmen antri and the dural covering of the temporal lobe. Next in fre¬ 
quency are the extradural spaces of the posterior fossa. 

Prognosis. —In cases in which adequate surgical drainage is provided 
before the subdural space has become involved, the prognosis is distinctly 
favorable. The amount of pus present does not seem to influence the 
prognosis, the evacuation of a large abscess by careful but free removal of 
diseased bone being followed usually by convalescence quite as rapid as 
in uncomplicated mastoiditis. Nor does the presence of granulations 
upon the involved dural surface seem to have any unfavorable prognostic 
significance,— i.e., always providing, of course, that the subdural space has 
escaped infection. 

The comparative frequency with which this lesion is discovered during 
operations upon the mastoid, the frequent absence of any characteristic 
symptoms, and the usually uneventful and rapid recovery after surgical inter¬ 
vention, all point to a very important fact in the pathology of suppurative 
lesions of the temporal bone,—namely, the remarkable power of resistance 
to the action of infective micro-organisms inherent in the intact dura mater. 

It has been intimated that a collection of pus in the posterior fossa 


340 


INTRACRANIAL LESIONS OF OTITIC ORIGIN 


constitutes a far more serious lesion than a similar collection involving the 
dural covering of the cerebrum. This is in part due to the fact that a deep- 
seated abscess in contact with the cerebellar dura may perpetuate itself by 
spreading thence through the aquseductus vestibuli or auditory nerve 
channels to the labyrinth (Hinsberg, Bezold); but to a greater extent its 
gravity is due to the fact that pus collections in this location are far less 
likely to be discovered during operation upon the mastoid. A considera¬ 
tion of this latter fact led Jansen to suggest the wisdom of exploring this 
region as a matter of routine practice in the operation of mastoidectomy. 

The treatment has already been indicated in speaking of the pathology 
of the disease. Careful removal of the diseased inner plate, or of the bone 
by which the pus is confined, is usually all that is required to convert 
the condition into one of simple uncomplicated mastoiditis. Usually the 
surgical treatment of extradural abscess forms part of an operation for 
the relief of suppurative mastoiditis. The technic will, therefore, be 
included in the description of the operation of mastoidectomy. 

PERISINOUS ABSCESS AND INFECTIVE SINUS PHLEBITIS. 

Perisinous abscess must in so considerable a proportion of cases be 
the immediate precursor of sinus thrombosis or phlebitis that there is every 
reason why the two conditions should be considered together. Only by 
such arrangement can the preventive treatment of the graver lesion—so 
far as prophylaxis is here possible—be duly emphasized. 

Perisinous Abscess.—This term is applied to an extradural abscess in¬ 
volving the dural covering of the lateral or sigmoid sinus. In its commonest 
form, it is simply a collection of pus confined between the dural surface of 
the sigmoid sinus and the grooved or arched plate of bone which separates 
it from the interior of the mastoid process. 

In its etiology and pathology a perisinous abscess does not differ 
materially from a similar (i.e., extradural) abscess in other situations. 
There are, however, certain features of dural arrangement which render 
this particular lesion especially dangerous to the patient, unless promptly 
relieved by surgical means. These anatomical features have so practical a 
bearing upon the possible course of the disease as to call for brief description. 

The dura covering the lateral convex surface of the brain is an exceed¬ 
ingly tough and resistant structure, very loosely adherent to the inner 
plate of the skull except along certain definite lines of attachment,—viz., 
along the lines of the principal sutures and at the edges of the groove for 
the lateral and sigmoid sinuses. In the region of the large venous sinuses, 
however, the dura divides into two layers, one of which lines the bone and 
forms the outer wall of the sinus, the other layer forming its inner wall. In 
the formation of the lateral sinus,— i.e., from torcular to knee,—the inner 
layer of the dura lining the mid-cranial fossa joins with the inner layer of 
the dura lining the posterior fossa to inclose the sinus, and from this point 
they are continued inward as the tentorium cerebelli. In the formation of 
the sigmoid portion of the sinus, the outer layer of the dura is attached 



PERISmOUS ABSCESS 


341 


rather firmly to the edges of the sigmoid groove, between which it lines the 
groove and forms the outer wall of the sinus. The inner layer is stretched 
rather tightly across the groove and thus forms the inner sinus wall. 

The influence of the anatomical arrangement above described upon 
the possible course of a perisinous abscess must be obvious. Taking for 
purposes of comparison an extradural abscess in the mid-cranial fossa, it is 
clear that pus may spread widely between the parietal plate and the dura 
covering the temporal lobes, and meet with little or no resistance. On the 
other hand, pus between the dural surface of the sigmoid sinus and its 
bony capsule finds the following conditions: (1) Dura of only half the 
usual thickness, and in which any inflammatory process more quickly 
involves the inner coat. (2) More or less firm attachment of dura on either 
side to the edges of the sigmoid groove, pus being forced to travel toward 
either torcular or jugular bulb, or to cause marked compression of the outer 
wall. That such compression may be extreme is definitely proved by six 
cases recorded by Passau, in each of which the vessel was actually occluded, 
the sinus walls being in contact and circulation wholly cut off by the pres¬ 
sure of an extradural collection of pus. 1 (3) The inner dural wall being 
tense and inelastic, any degree of compression of the outer wall must tend 
to retard the venous flow and possibly increase friction,—either condition 
favoring the formation of a thrombus within the vessel. (4) Pus thus 
confined may cause softening of the sinus wall at any point, thus providing 
a pathway of infection leading to infective sinus phlebitis; or it may per- 



Fig. 189. — Semi - diagram¬ 
matic picture showing section 
of sigmoid sinus and separation 
of dural layers. 



Fig. 190. — Showing perisi¬ 
nous abscess, the thinness of 
the dural coat favoring perfora¬ 
tion and intra-sinus infection. 



Fig. 191.—Showing possible 
pathways of infection by sim¬ 
ultaneous perforation of outer 
and inner coats, leading to in¬ 
fection both of sinus and cere¬ 
bellum. 


forate simultaneously the two layers of dura at the point of their attach¬ 
ment to the edge of the sigmoid groove, carrying infection both to the 
sinus and to the cerebellum beneath (Figs. 189, 190, and 191). Possibly 


1 Passau’s Beitr., Bd. 3, Heft 1 and 2, 1910. 














342 


INTRACRANIAL LESIONS OF OTITIC ORIGIN 


in this way may be explained the large number of cases seen or reported in 
which infective thrombosis and cerebellar abscess have apparently de¬ 
veloped coincidently. 

The author does not wish to convey the impression that he regards pen- 
sinous abscess as likely in most cases to lead quickly to the above very 
serious infections. As practical aural surgeons we know, from the many 
cases which have come under our personal observation, that a perisinous 
abscess may exist for a considerable period may even produce a local¬ 
ized pachymeningitis, as evidenced by granulations covering the dura— 
without involving either the interior of the sinus or any subdural structure. 
With due consideration of these facts, we must not forget that the tendency 
of such a lesion, if not relieved by surgical means, must be to invade sooner 
or later either the sinus or the cerebellum, or both. It is of the greatest 
importance, therefore, that such an abscess be evacuated early, i.e., 
before it shall have given rise to a more serious lesion. 

If we may draw any practical deductions from the above, they may be 
stated somewhat as follows: 

(1) Whenever in a case of suppurative mastoiditis the symptoms have 
been such as to suggest the possibility of sinus infection, the sinus should be 
uncovered. In ordinarily skilful hands, this exposes the patient to no 
additional risk, and, even if no abscess be found, we shall at least have 
eliminated one source of danger. 

(2) When in an operation for acute mastoiditis an unsuspected and 
unusual amount of pus is encountered,— e.g., pus flooding the mastoid cells 
proper, the zygomatic cells, and possibly also the cells further back toward 
the occipital border,—it is safe and conservative surgery to expose the 
sigmoid sinus in order to eliminate the possibility of an abscess in this 
location. 

(3) When physical changes are present leaving in doubt the health of 
the sinus groove, this bone should be removed. An exposed sinus is un¬ 
questionably a safer condition than a sinus in contact with bone the power 
of which to maintain its own nutrition is in doubt. 

Symptoms. —The symptoms of uncomplicated perisinous abscess are 
so indefinite as to call for but brief mention. When the amount of 
pus between dura and sinus groove is small, there are usually absolutely 
no symptoms other than those which may occur with uncomplicated 
mastoid disease. With a large perisinous abscess there may be some 
evidences of sepsis simply as a result of the extended surface for 
pus absorption. Usualty, however, there are no symptoms upon which 
one could possibly base a diagnosis of the lesion under discussion. 
Frankly, there is no chain of symptoms characteristic of uncomplicated 
perisinous abscess. 

As with extradural abscesses in the mid-cranial fossa, perisinous ab¬ 
scesses are usually discovered during the course of a mastoid operation, 
either accidentally or through exploratory exposure for one or other of the 
reasons outlined above. 


INFECTIVE SINUS PHLEBITIS 


343 


On removing the bone covering such a lesion, the conditions found 
may vary both as to the amount of pus and as to the state of 
the exposed dura. There may be, for example, only a few drops 
or a very considerable amount of pus,— the larger amount having no 
unfavorable significance as to the prognosis, provided the sinus wall 
is found to be healthy. The dura may appear quite normal even in 
the presence of an abscess of considerable size. On the other hand, 
it may show various physical signs of disease,— e.g., it may be covered 
by granulations or may present the characteristic changes of superficial 
erosion. These structural changes of the dural wall do not, however, 
properly belong to this lesion, since they constitute rather the early 
changes in sinus phlebitis. 

A point, however, which can not be too strongly insisted upon is this, 
that the presence of visible changes in the outer surface of the dura— e.g., 
granulations, slight surface erosions, etc.—furnishes no proof that the 
vessel wall is diseased through its entire thickness or that the interior of 
the sinus has become infected. 

Prognosis.—A perisinous abscess without noticeable changes of the 
dura, and which has received adequate surgical treatment, offers a per¬ 
fectly favorable prognosis. Even in the presence of inflammatory changes 
in the sinus wall, the prognosis is usually favorable, unless there are accom¬ 
panying symptoms of periodic septic absorption. 

From what has been said we may deduce the chief indication of treat¬ 
ment,— viz., the evacuation of pus by careful removal of the overlying 
bone. It is not sufficient to create a small opening through which pus may 
escape, the greatest safety being provided by a rather extensive uncover¬ 
ing of the sinus,— i.e., certainly by a removal of bone coextensive with the 
size or extent of the abscess. 

Granulations upon the dura are to be regarded as part of Nature s 
process of repair. Not on any account should they be curetted. On the 
contrary, the greatest care should be observed not to disturb or injure 
them, since a slight traumatism may convert a comparatively simple, 
lesion into one of serious intra-sinus infection. 

The surgical technic for exposing and draining a perisinous abscess 
forms part of the operative treatment ol suspected sinus phlebitis, and 

will be described in detail in a later chapter. 

Infective Sinus Phlebitis; Suppurative Thrombophlebitis of the Sig¬ 
moid or Lateral Sinus; Sigmoid Sinus Thrombosis. I he word phlebitis 
means literally an inflammation of a vein. Any inflammatory process 
— e.g., the superficial changes so often discovered accidentally during 
mastoid surgery—should, therefore, fall under this heading. Practically, 
however, such a lesion causes recognizable symptoms only when the 
infection has involved the intima as well as the outer coats of the vessel. 
The term infective sinus phlebitis, being associated with a definite symp¬ 
tom complex, has come to apply in otology only to a lesion producing 
intra-sinus infection. And since an infective process involving the inner 


344 


INTRACRANIAL LESIONS OF OTITIC ORIGIN 


coat of the lateral or sigmoid sinus very frequently gives rise to the forma¬ 
tion of a thrombus at the site of the lesion, the terms, “ infective sinus 
phlebitis,” and “sinus thrombosis” were formerly regarded, and in oto- 
logical parlance and literature were used, as practically synonymous. Of 
late years, however, we have come to recognize that the lesion resulting 
from intra-sinus infection may take the form of two pathologically distinct 
conditions, viz., infective* clot formation (infective sinus thrombosis) and 
infective changes of the inner coat without clot formation (infective sinus 
phlebitis). 

Etiology. —In the cases preceded by perisinous abscess, the causes 
are naturally in large degree those of the intermediate lesion. We have 
seen, however, that in many cases perisinous abscess does not give rise 
to intra-sinus infection. After an extradural effusion of pus has taken 
place, therefore, there must be certain factors which bear upon the prog¬ 
ress of the lesion, and which determine whether it shall remain circum¬ 
scribed or rapidly invade the sinus. 

Probably changes in the individual s powers of resistance to disease 
furnish the determining factor in many cases. There can be no doubt, for 
example, that children suffering from suppurative middle-ear lesions com¬ 
plicating the acute infectious diseases more frequently develop intra-sinus 
infection than do children who have not been subjected to such severe 
systemic depletion. A very large percentage of the cases of infective sinus 
thrombosis which have come under the personal care of the writer have 
been among patients whose aural lesions have occurred either as a com¬ 
plication or sequela of severe constitutional disease. 

The character of the infection is also a most important etiological 
factor in purulent sinus phlebitis. Leutert, in studying the bacteriology 
of cases of aural infection requiring operation, found in a large series 
that the streptococcus was responsible for all cases of infective sinus 
thrombosis. This view had the support of Bezold, who stated that in all 
cases of sinus infection examined in his hospital practice the streptococcus 
was found. Further rather positive corroboration of this conclusion is found 
in the careful studies of Dr. Librnan in the Mt. Sinai Hospital of New York. 

Pathology— From the macroscopic appearances disclosed by surgical 
exposure of the sinus, it would seem that the morbid changes leading to 
infective sinus phlebitis may originate in two conditions,—viz., either (a) 
the presence of extradural pus,— i.e., perisinous abscess; or (b) contact of 
dura with diseased bone. The latter may be assumed when no fluid pus is 
found between dura and bone, the two being simply soldered together 
through inflammatory adhesions. In either case the changes in the sinus 
wall probably follow each other in much the same order. Arguing an 
analogy between this lesion and similar processes elsewhere in the body 
we may assume that the dura in contact with diseased bone, or separated 
from it only by fluid pus, undergoes sooner or later the changes character¬ 
istic of an acute exudative inflammation; i.e., first dilatation of the minute 
blood-vessels and subsequent retardation of the blood-current; next. 


INFECTIVE SINUS PHLEBITIS: SYMPTOMS 


345 


transudation of serum and migration of leucocytes from the veins into the 
surrounding tissues. Unless quickly relieved, there is a proliferation of 
new cells, and the surface layer of endothelial cells undergoes necrosis. 
Upon this denuded surface granulations soon form. This probably repre¬ 
sents a reparative stage of the lesion in which prompt and skilful surgical 
treatment results in the great majority of cases in fairly rapid resolution 
and recovery. The vessel wall is now thickened by the products of an 
acute exudative inflammation, but from further infection it is guarded by 
a protective layer of granulations. Removing from contact with these 
granulations all inflamed or necrotic bone, we pave the way for prompt 
recovery. Without such surgical relief, the lesion may progress in one of 
two ways,—viz., prolonged contact with the products of suppuration 
leads to necrotic softening of the vessel wall in its entire thickness at some 
point, thus providing a pathway of infection to the interior of the vessel; 
or the pressure upon the vessel wall by pus or by exuberant granulations 
may cause marked narrowing of its lumen at the point of the lesion, this 
leading to inflammatory changes of the intima. By whatever step the 
inner coat becomes involved in the inflammatory process, the mechanical 
result must be one or other of two conditions, viz., (1) the development of 
an intra-sinus erosion and clot at the site of the lesion (infective sinus throm¬ 
bosis); or (2), in the absence of actual or demonstrable clot formation, the 
infection may involve and spread beneath the inner coat which, becoming 
eroded at one or several points, provides the means for periodic infection of 
the general blood stream (infective sinus phlebitis). It is essential that we 
recognize these two conditions as theoretically separate lesions in order (a) 
to explain the symptoms in those cases in which no clot is macroscopically 
demonstrable during operation; and (b) to give at least theoretic force to the 
contention of those surgeons who claim that resection of the jugular vein, 
rather than ligation, may in some cases be necessary and therefore is the 
safer routine procedure. 

The first stages of clot formation may be accompanied by no clinical 
disturbances,—this being accounted for by the lacu that the thrombus is 
probably always parietal at the start, and whatever germs it may imprison 
are at first imbedded within a firmly organized coagulum, and only reach 
the general current of the blood at a later priod when the clot shad have 
reached the stage of gradual disintegration. 

Symptoms. —-Considering under this head all conditions, subjective oi 
objective, which may possibly throw light upon this lesion, it would seem 
logical to look for symptoms falling under the following heads: 

’’(l) Symptoms due to periodic discharge of septic matter into the 

general circulation. 

(2) Symptoms due to disturbance of cerebral circulation,—probable only 
in thecaseof a clot producing absolute obstruction. While complete occlusion 
is not particularly rare, definite symptoms, clearly attributable thereto, are. 

(3) Bacteriamiia, or the demonstration of pus germs in the general 

blood current. 



346 


INTRACRANIAL LESIONS OF OTITIC ORIGIN 


(4) Physical signs (often completely absent). 

(5) Physical changes in the sinus wall, surgically exposed for in¬ 
spection. 

(6) Evidences of secondary foci of infection (abscesses) due to 
metastasis. 

Symptoms of Periodic Septic Absorption .—There is probably no recog¬ 
nized lesion in which the chief clinical phenomena are more clearly the 
expression of the morbid changes present than in sinus thrombosis. As 
stated before, the formation of a firm parietal clot— i.e., a clot adherent 
to the sinus wall and not obstructing its lumen—may produce absolutely 
no symptoms. Should such a clot be sterile,— i.e., contain no pathogenic 
bacteria,—it may become organized into fibrous tissue, and never give 
rise to symptoms by which its presence might become known. How often 
this actually occurs, there is no means of determining. Presumably, 
however, most thrombi resulting from a suppurative process in contact 
with the outer sinus wall themselves contain the germ which has been 
the original source of infection. In this condition we may have a clot, 
peripherally sterile, but containing a central focus of infection, which 
finally leads to suppurative disintegration, with sudden propulsion of 
septic matter into the general blood stream. It is not surprising that the 
first definite symptoms are usually sudden, characteristic, and pronounced. 

The symptom which first attracts the physician’s attention is sudden 
and very marked rise of temperature. The temperature which has been 
hugging the normal line, or rising only slightly above it, suddenly shoots 
upward to 103° or even 105°F. Simultaneously the pulse-rate is increased, 
— e.g., from 80 or 85 to 110 or 120 beats per minute in adults, or to a much 
higher rate of rapidity in children. During the period of pyrexia the patient 
is flushed and has the appearance of being exceedingly ill, as indeed he 
really is. During this stage he may complain of severe headache, this, 
however, in the writer’s experience, being exceptional rather than the rule. 
The temperature, after maintaining its higher level for a few hours, suddenly 
begins to fall, and then drops rapidly to the normal line or a little above it. 
The fall of temperature is often accompanied by profuse sweating. He 
now enters upon an afebrile period of variable length, during which he 
feels comparatively well and comfortable. This sense of comparative ease 
and physical well-being is so commonly present and is in many cases so 
pronounced as to constitute one of the characteristic features of the disease. 
Unfortunately, this period of comfort and freedom from fever is distinctly 
limited. Usually in 24 hours, but in some cases not until two or three 
days have elapsed, the temperature again mounts rapidly to a point near or 
above the previous high level. The symptoms of the first febrile attack are 
now repeated, to subside rapidly after a few hours as the temperature again 
falls to the normal line. From this time the clinical course of the disease 
usually assumes a markedly periodic character, high fever and remission 
succeding each other often at fairly regular intervals. 

In some cases before each rise of temperature the patient experiences a 


INFECTIVE SINUS PHLEBITIS: SYMPTOMS 


347 


pronounced chill, or rigor, which may be so pronounced as to be quite 
noticeable to nurses and attendants, and may last from five to ten min¬ 
utes, or considerably longer. More often a distinct chill is not repeated, 
the patient complaining simply of a sense of chilliness just before the attack. 
In some cases neither a chill nor a sense of chilliness is complained of. 

The blood count in septic sinus thrombosis, so far as has been observed, 
follows the same general laws which govern its changes in other suppurative 
lesions. The statement of Crockett, 2 that a gradual and progressive increase 
in the number of white cells to a point not usually exceeding 20,000 is a 
characteristic feature in septic sinus phlebitis, is of interest, and, if verified 
by further observation, will be of diagnostic value. 

The cycle of septic phonomena above described undoubtedly forms 
the basis of one’s diagnosis in the great majority of cases. It is clear 
that the two components of each febrile paroxysm are the logical results 
of the morbid process within the sinus,—the sharp rise of temperature 
marking entrance into the blood stream of septic mattei from the 
disintegrating thrombus; the rapid fall to normal indicating their final 
elimination, or the final exhaustion of their toxic agents. In addition to 
the periodic character of the attack, the patient shows always a progressive 
loss of flesh, strength, and “tone,” finally assuming the characteristic 
“septic look” which is so difficult to describe but usually so unmistakable 


to the practised eye. 

The symptoms traceable to disturbed cerebral circulation are more often 
absent than present, and may be dealt with briefly. Crockett alludes 
to headache, nausea, and vomiting as among the occasional symptoms 
of sinus thrombosis. Headache of rather severe type may be present 
during the height of the febrile attack. Occurring during the period 
of remission, it is more likely to be due to the cerebral congestion caused by 
an obstructive clot. In two cases reported by Gruening 3 the sinus was 
absolutely occluded by an obstructive thrombus, and in each case the patient 
exhibited marked mental lethargy and drowsiness, one patient lapsing quickly 
into somnolence as soon as left undisturbed. Both of these patients suffered 
also from severe headache. In cases of parietal (i.e., non-obstructive) 

thrombosis the above symptoms are absent. . . * 

A symptom which is occasionally present in obstructive sinus thiom- 

bosis is optic neuritis. Its occurrence has been observed and recorded by 
Gruenino- Kipp, Crockett, Freidenberg, Jansen, and others. In ('rockett s 
series of 60 operable cases, taken from the records of the Boston Charita¬ 
ble Eye and Ear Hospital, optic neuritis was present in 16, or slightly over 
25 per cent. This is a larger percentage than has been recorded by other 

observers. 

Hvpersemia of the optic nerve, optic neuritis, or choked disk, in a case 
presenting other clinical evidences of sinus phlebitis, would point rather 


2 Crockett: Thrombosis of the Lateral Sinus, Annals of Otol., June, 1906. 

3 Gruening: Sinus Thrombosis of Otitic Origin and its Relation to Streptococcicmia, 

Annals of Otology, March, 1910. 







348 


INTRACRANIAL LESIONS OF OTITIC ORIGIN 


strongly to an obstructive lesion,— i.e., to a clot producing complete obstruc¬ 
tion. Absence of all ocular changes is, however, absolutely without signifi¬ 
cance as an indication that the sinus is not diseased. 

Most aural surgeons of large experience have seen cases of very extensive 
clot formation,—as, for instance, of a thrombus extending backwaid neatly 
to the torcular and downward so as to occlude the entire length of the jugular 
vein. In such cases it is easily conceivable that the thrombotic process 
may extend through the superior petrosal sinus to the cavernous sinus, 
practically obliterating the lumen of that vessel. Should this exceedingly 
rare complication occur, it would or might be announced by the following 
spectacular array of physical signs! oedema of the corresponding eyelids 
and about the brow, chemosis of the conjunctiva, exophthalmos and 
immobility of the eyeball from postorbital cellulitis. 

Bactericemia. —It has long been known or believed that most of the 
important clinical phenomena of infective sinus thrombosis are directly 
attributable to the passage of germs from a disintegrating clot into the 
general blood stream. It is surprising, therefore, that attention was not 
directed earlier to the importance of blood cultures in cases of suspected 
sinus infection. Impetus has in recent years been given to the study of 
this question in America by the careful investigations of Dr. E. Libman 4 
in the Pathological Laboratory of the Mt. Sinai Hospital of New York. 
The results of these investigations have corroborated the views ex¬ 
pressed by Leutert 5 and Suepfle, 6 —viz., that the great majority of cases 
of sinus thrombosis are due to a streptococcus infection. Suepfle, from 
a careful analysis of a large series of cases, expressed his belief that cases 
of staphylococcus and pneumococcus infection rarely give rise to any 
intracranial complication. Libman, writing in 1908, after searching the 
literature of the subject, found an absence of authentic records of cases of 
sinus thrombosis due to the pneumococcus. These laboratory reports have 
the clinical support of Professor Bezold, 7 who stated in his text-book of 
otology, that all the cases of sinus thrombosis operated upon by him in his 
hospital practice were cases of streptococcus infection. A most interesting 
contribution to our clinical knowledge of the bacterisemia of sinus throm¬ 
bosis is found in a paper by Dr. Emil Gruening, published in the New York 
Medical Journal of June 5, 1909. This paper is based upon 10 cases 
lateral sinus thrombosis operated upon by him in the Mt. Sinai Hospital 
and the results of the blood examinations by Dr. Libman. The blood for 
these cultures was taken from the median basilic vein. These examinations 
gave positive results in seven cases, being negative in the other three. 
“The micro-organisms causing the infection were in five cases the strep- 

4 Libman: Value of Bacteriological Examinations in Otology, with Special Refer¬ 
ence to Blood Cultures, Arch, of Otol., xxxvii. 

5 Leutert: Bakteriologisch-Klinische Studien liber Complicationen Acuter und 
Chronischer Mittelohreiterungen, Arch. f. Ohrenheil., Bd. 46, p. 190. 

6 Suepfle: Cited by Libman, ibid. 

7 Bezold: Text-book of Otology, p. 157. 





INFECTIVE SINUS PHLEBITIS: PHYSICAL SIGNS 349 

tococcus pyogenes, in one case the streptococcus mucosus, in another the 
bacillus proteus. The same organisms had previously been found in the 
purulent discharge from the ear.” Further proof of the practical value of 
blood examinations under certain circumstances is found in two cases, 
also reported by Dr. Gruening, in which, with no previous history of ear 
trouble, the sinus was explored solely on the strength of characteristic 
symptoms of septic absorption and a demonstrable streptococcaemia, an 
infected thrombus being found in each case. 

A less positive conclusion as to the value of blood cultures as a means 
of determining septic sinus thrombosis seems deducible from the results 
published in the same year by Drs. Arthur B. Duel and Jonathan Wright, 
writing in collaboration. 8 Their report is based upon a series of 57 cases, 
treated in the wards of the Manhattan Eye and Ear Hospital, in which 
careful blood examinations were made. Of these 57 cases a positive bac- 
terisemia was found in 16. Of the 16 positive blood cultures, streptococci 
were present in 14, pneumococci in 2. Analyzing them further, according 
to the lesions present, we find that 4 were characteristic cases of septic 
sinus thrombosis, 1 of suppurative labyrinthitis with leptomeningitis, 2 
were of frontal sinusitis, and the remaining 9 cases were of uncomplicated 
mastoiditis which made uneventful recoveries following simple mastoid¬ 
ectomy. 

Clearly there are certain facts which should be thoroughly weighed and 
digested before arriving at a conclusion as to the surgical significance of a 
demonstrable streptococcsemia in cases of middle-ear suppuration. These 
facts may be marshalled somewhat in the following order: 

Bacteriiemia is a usual accompaniment of septic endocarditis; it is not 
infrequently present in pneumonia and in purulent meningitis, it may be 
present in severe cases of tonsillar infection; it occurs not infrequently in 
the septic type of scarlet fever. It may, according to Duel and Wright, 
be present in cases of uncomplicated suppuiati\e mastoiditis. 

Libman’s paper 9 is a perfectly fair and scientific statement of his 
results in an exceptionally brilliant series of cases. His investigations 
have helped to place at our disposal a very valuable aid in the diagnosis 
of doubtful cases. It does not appear, however, even when no other focus 
of infection can be located, that the mere presence of streptococci m the 
blood, unless reinforced by clinical manifestations of the disease, can be 
accepted as sufficient grounds for diagnosticating sinus thrombosis or for 

opening the sinus. . . . 

Physical Signs —There are no constant physical signs of infective 

sinus thrombosis. In some cases of acute sinus phlebitis, the inflammatory 
process spreads backward along the mastoid vein to its point of entiance 
at the mastoid foramen, causing noticeable tenderness at this point. The 
position of this foramen varies somewhat, being usually about 1M to 1/2 

8 Duel and Wright: Clinical and Pathological Significance of Bacteriaemia m 
Suppurative Otitis, N. Y. Med. Jour., Oct. 30, 1909. 

Libman: loc. cit. 




350 


INTRACRANIAL LESIONS OF OTITIC ORIGIN 


inches behind the orifice of the cartilaginous meatus and on a level with 
its floor. Clearly defined sensitiveness to pressure at this point is legarded 
by some surgeons as a valuable diagnostic sign of sinus phlebitis. It is a 
condition which may easily be simulated by an extension of inflammation 
backward through a pneumatic mastoid to the large pneumatic spaces 
frequently present in this region. 

Sensitiveness to pressure along the course of the jugular vein may be 
caused by an extension of inflammation to the jugular bulb and thence along 
the walls of the vein. When this inflammation is pronounced, the surround¬ 
ing tissues may become involved, giving rise to a noticeable induration under 
the sternomastoid muscle. As a further extension of this secondary in¬ 
flammation, the cervical glands lying in front of and behind the sterno¬ 
mastoid muscle may be distinctly enlarged. 

The recognition by deep palpation of a cord-like mass supposed to repre- 
sent a thrombus filling the jugular vein, has been mentioned by many au¬ 
thorities as a valuable physical sign in cases of extensive clot formation. 
Personally I have never been able to recognize it. One reason for my failure 
may be the fact that I have always believed that any forcible or deep 
palpation along the course of the vein in cases of suspected jugular throm¬ 
bosis is an exceedingly unwise and dangerous procedure. It is conceivable 
that one might easily in this way dislodge and force into the general blood 
current a large portion of the infected clot, giving rise not only to pro¬ 
nounced systemic poisoning, but possibly also to disseminated metastatic 
foci of infection. 

Moderate induration along the course of an infected vein, resulting 
from inflammatory changes in the surrounding tissues, is not very uncom¬ 
mon, and when present is an easily recognized and very valuable diag¬ 
nostic sign. The writer is inclined to believe that this condition has in 
many cases been misinterpreted as representing an organized clot within 
the vein. 

Macroscopic Changes m the Sinus Wall. —In a case of suspected sinus 
thrombosis, the exposure of the sinus for the purpose of inspecting its 
outer wall is not only justifiable, but clearly called for. Removal of the 
overlying bone may reveal one or more of the following conditions,—viz., 
(1) Inflammatory adhesions between bone and dura. This in some cases ren¬ 
ders the uncovering of the sinus somewhat difficult and is an occasional 
cause of its accidental rupture. (2) The presence of fluid pus in contact 
with an apparently healthy sinus. This condition (perisinous abscess) is 
not particularly uncommon, and in adults may give rise to no symptoms 
whatever. In the case of young children, on the other hand, a perisinous 
abscess may cause a temperature of very septic type,— i.e ., sudden high 
rises alternating with remissions. I have seen a large number of such cases 
among children suffering from scarlet fever in the wards at the Willard 
Parker Hospital. The whole clinical picture may be such as to suggest 
intra-sinus infection. These symptoms usually subside after removal of 
the diseased bone,—unless, of course, there be a focus of infection within 


INFECTIVE SINUS PHLEBITIS: PHYSICAL SIGNS 


351 


the sinus. (3) Presence of granulations upon the dura. In addition to 
perisinous abscess, we frequently find the dura covered by a layer ol granu¬ 
lations. With this condition the sinus wall may be very considerably 
thickened. Granulations do not form upon the normal dura. Their mere 
presence, therefore, is evidence of inflammatory changes involving at 
least the outer coats of the vessel. Such inflammatory changes with the 
superimposed granulations must necessaiily mean thickening and in¬ 
creased resistance to pressure in that part of the sinus wall covered by 
granulations. In general, the increase in rigidity is proportional to the 
duration of the lesion. It does not necessarily follow, however, that the 
inner coat of the vessel is involved, and there is reason to believe that in a 
majority of cases such involvement does not take place if surgical inter¬ 
vention is not too long postponed. The point I wish to make is, that, 
wherever granulations are found, the sinus wall must be thickened and must 
offer increased resistance to the palpating finger. Unless the surgeon 
realizes this fact, he may receive the impression that he has under his finger 
a parietal clot and be led into the mistake of opening a sinus which Nature 
is guarding from infection, and which requires only the removal of super¬ 
imposed diseased bone to insure a rapid recovery. (4) Inflammatory 
changes with absence of gramdations. Conditions presenting even greater 
difficulties of interpretation are extensive inflammatory changes, occa¬ 
sionally encountered, with little or no tendency to the formation of pro¬ 
tective granulations. Every aural surgeon of considerable experience will 
recall the anxiety which such cases have occasionally caused him. The 
sinus wall may present (a) a dull sodden, somewhat oedematous, or water¬ 
logged appearance, the moderate lustre characteristic of normal dura 
being lost, and the usual bluish-gray color being changed to a somewhat 
purplish hue. The impression received is of an extensive pathologic 
change involving the entire thickness of the vessel wall. Or (b) the sinus 
wall may appear thinner than normally, and its normal lustre may have 
given place to an unnaturally glazed appearance. The macroscopic appear¬ 
ance is of marked atrophy, giving the impression of a tissue whose power 
of maintaining its own nutrition has been either destroyed or reduced to 
a minimum. Wlien a sinus presenting this appealance conveys also a 
positive sense of resistance to the palpating fingei, it is not suipiising that 
the surgeon should suspect the presence of an adjacent clot. Again, (c) theie 
may be areas of superficial erosion. This loss of surface epithelium may 
represent a traumatic result, marking the site of a formei adhesion between 

the inflamed dura and the removed bone. 

The writer at the present writing has under his care in one of the 
scirlet fever wards of the Willard Parker Hospital an adult patient whose 
sinus wall showed in different parts two of the conditions above described. 
The mastoid lesion was one of rapid and very extensive osseous necrosis. 
The sinus wall presented alternating areas of appa.ent atrophy and mfiltia 
tion in different parts, and as a whole appeared so devitalized and extensively 
diseased that the writer predicted that the subsequent course of the lesion 


352 


INTRACRANIAL LESIONS OF OTITIC ORIGIN 

would prove the interior of the vessel to have become infected. There had 
been however, no symptoms altogether typical of septic poisoning through 
the sinus, and it was decided to keep the patient under observation for a 
day or two before subjecting him to further operative intervention. Since 
then ten days have elapsed, and no symptoms of further septic absorption 
have occurred. The diseased sinus is now covered with protective granu¬ 
lations and the patient is on the road to recovery. 

It may seem from the above that the writer is devoting much space to 
a discussion of conditions having little bearing upon sinus thrombosis 
That is not exactly the case. The physical conditions above described 
lead, if not surgically relieved, to infective sinus thrombosis. They form, 
therefore, a stage in the pathology of that lesion. The infective process 
may already have reached the inner coat of the vessel. We can not be 
sure, however, that intra-sinus infection has actually occurred unless, in 
addition to the physical changes above described, there are also some 

constitutional evidences of septic absorption. 

As to the form of pathologic change in the sinus wall which may be 
accepted as positively indicating intra-sinus infection either present or 
inevitably to follow, my experience does not justify me in describing under 
this head any condition short of obvious gangrenous destruction of its 
vitality at some point. In short, while there undoubtedly are cases which 
justify the surgeon of large experience in opening the sinus upon the physi¬ 
cal changes alone, the writer believes that they are exceptional. Certainly 
the surgeon whose experience with sinus lesions has not been large should 
not operate upon the sinus in the absence of characteristic symptoms of 
periodic sepsis. 

Aspiration Movements .—Before leaving the discussion of physical 
changes, a word should be said of the so-called respiratory, or aspiration, 
movements occasionally seen in an exposed sinus. 

The large veins of the neck, and notably the internal jugulars, show 
normally, if exposed surgically, very marked variations in calibre which 
occur synchronously with the respiratory movements. Thus, an exposed 
internal jugular balloons out during deep expiration and collapses during 
inspiration. These movements of the vein—exaggerated during forced 
respiratory efforts—are naturally less conspicuous during quiet respira¬ 
tion. Since the internal jugulars represent the direct continuation of the 
sigmoid sinuses, one would expect to observe similar movements of the 
latter when exposed during operation. Ordinarily, however, the sinus does 
not participate in these movements, sudden changes in its calibre being- 
guarded against by various factors, prominent among which are the marked 
constrictions above and below the jugular bulb, and the sharp angular 
bends which obstruct the current in the neighborhood of the jugular 
foramen. When, however, the current is cut off by an obstruction ( e.g ., 
clot) at the torcular end of the canal, the blood-pressure is so far reduced 
that noticeable collapsing of the sinus wall, synchronous with inspiration, 
occurs in that portion of the vessel between the obstruction and its exit 


INFECTIVE SINUS PHLEBITIS: PHYSICAL SIGNS 353 


at the jugular foramen. Such a phenomenon in a case of suspected sinus 
thrombosis would, therefore, suggest an obstructing clot situated between 
the exposed sinus wall and the torcular. While its occasional occurrence 
and possible significance should be kept in mind, it is not a trustworthy 
sign, its unreliability being due mainly to two facts,—viz.: (1) If the 
obstruction were far back,— i.e., posterior to the entrance of the superior 
petrosal sinus, the blood from this sinus and from the mastoid emissary 
and posterior condyloid veins might be sufficient to maintain the usual 
pressure and prevent aspiration movements; and (2) with absolutely no 
clot or obstruction in any part of the sinus, moderate aspiration movements 
may be present in a perfectly normal vessel. In a case of mastoiditis 
operated upon some years ago by the writer, the wall of the exposed sinus 
showed not only well-marked pathologic change but also noticeable, 
almost flapping movements synchronous with the respiratory movements. 
This case, after causing the writer considerable anxiety, went on to unevent¬ 
ful recovery. This phenomenon in an unobstructed sinus I can account for 
only upon the hypothesis of an unusually large jugular foramen and a very 
large jugular vein which exerts during inspiration an unusually forcible 
drag upon the blood current in the sinus. 

The course of the disease, after a focus of infection within the sinus 
has been established, is one of gradual, but ever progressive, loss of strength 
and vitality. The remarkable absence of symptoms, either subjective or 
objective, which usually characterizes the periods of remission during the 
early days of the attack, becomes gradually less marked as the patient 
becomes more and more septic. With the repeated entrance of septic 
emboli into the general blood stream, metastatic abscesses may be estab¬ 
lished in various parts of the body. I have seen such abscesses over the 
sternum, at the wrists, elbows, knees, or ankles. I have seen four or five 
such abscesses develop almost simultaneously in the same patient. In 
like manner, septic matter may find lodgement either in the lung or heart, 
giving rise to a septic pneumonia or to a septic endocarditis. In a case suc¬ 
cessfully operated upon by Dr. John B. Rae 10 for septic sinus thrombosis 
of the right side, the patient later developed symptoms of brain abscess 
in the left hemisphere, which was subsequently opened and drained. The 
cases cited indicate to some extent the multitude of dangers which hover 
about the patient suffering from this lesion, and which are ended only 
when the focus of infection within the sinus has been eliminated or its 
connection with the general circulation has been cut off. While the devel¬ 
opment of metastatic abscesses subjects the patient to intense suffering 
and increases enormously the drain upon his vitality, they do not render 
the prognosis hopeless. In one of the last cases operated upon by the 
writer, and in which he was obliged to resect the jugular vein, there was a 
large metastatic abscess involving the right elbow, which did not, however, 
interfere appreciably with the patient’s rather rapid recovery. In a single 


10 Rae: Transactions Am. Otol. Society, 1911. 
23 




354 


INTRACRANIAL LESIONS OF OTITIC ORIGIN 


case operated upon by Gruening, 11 metastatic abscesses developed and 
were successively evacuated in the right thigh, the right knee, the posterior 
aspect of each arm, the perineum, and last in the suprapubic region, the 
patient finally making a complete recovery. 

Before making a diagnosis of sinus thrombosis, it is of course essential 
that all other diseases which might cause like symptoms should be defi¬ 
nitely excluded. Among such may be mentioned pneumonia, typhoid 
fever, acute endocarditis, malaria, and certain cases of scarlatinal infection. 
The distinguishing features by which these conditions may be differentiated 
are known to all experienced physicians, errors in diagnosis being more 
likely to result from a too narrow conception of disease on the part of the 
aurist than from the absence of symptoms or physical signs which the 
trained diagnostician might be expected to detect. It is worthy of note 
that all the conditions referred to above are diseases in which a bacteri- 
semia is known occasionally to occur. 

In the writer’s experience, the cases presenting the greatest difficulties 
of diagnosis are those of children suffering from the septic type of scarlet 
fever. That such cases occur without any discoverable focus of localized 
infection is a fact well known to physicians in large practice among chil¬ 
dren. I have seen cases in which the temperature has for days run a course 
altogether characteristic of intra-sinus infection, but which have ulti¬ 
mately recovered without operation. With such facts in mind, the coinci¬ 
dence of severe scarlatinal infection and suppurative otitis media involves 
a problem of no little difficulty. At first thought, it would seem that such 
cases are pre-eminently of the class in which the examination of the blood 
from a distant vein for evidences of bacterisemia would be of the greatest 
value. Unfortunately, the infectious diseases—and particularly scarlet 
fever—are known, even in the absence of sinus involvement, to be an occa¬ 
sional cause of streptococcaemia. Blood cultures are, therefore, not of very 
positive value in locating the principal focus of infection in cases of sepsis 
complicating the acute infectious diseases. 

Prognosis. —We shall speak more intelligently of the prognosis if 
we accustom ourselves to recognize two distinct stages of the lesion,— 
viz.: (1) suppurative sinus phlebitis externa , characterized by inflammatory 
changes involving only the outer coats of the sinus wall; and (2) infective 
sinus phlebitis interna , or—since inflammation of the inner coat is usually 
coincident with clot formation — infective sinus thrombosis. Unless 
relieved by some form of surgical intervention, the prognosis in any stage 
of the disease is exceedingly unfavorable. Even when the inflammation 
is confined to the outer dural surface, it is difficult to conceive how resolu¬ 
tion can take place, or intra-sinus infection be averted, so long as the dura 
is in contact with diseased or necrotic bone or bathed by confined pus. 
As soon, however, as we have removed all diseased structures from con¬ 
tact with the inflamed dura, we have paved the way for the processes of 


11 Gruening: Annals of Otol., March, 1910, pp. 148-151. 



INFECTIVE SINUS PHLEBITIS: TREATMENT 


355 


repair, and in most cases for fairly rapid recovery. In the great majority 
of cases intra-sinus infection does not subsequently take place. 

In the second stage— i.e., after a focus of infection within the sinus 
has been established recovery without further operative intervention 
can not be expected. 

Treatment. The treatment of this lesion is purely surgical. That 
of the first stage i.e., before the interior of the sinus has become involved 
is practically the same as that already advocated for perisinous abscess, 
viz., the removal of all diseased bone from contact with the inflamed 
dura. In carrying out this provision, we have tw r o surgical guides as to the 
extent to which the sinus should be uncovered,—viz., (1) until apparently 
normal dura is reached in both directions,— i.e., toward the torcular and 
if possible tow r ard the bulb; and (2) until the bone in contact with the 
sinus in all directions is perfectly sound and healthy. It is better to remove 
rather too much than too little, if by the latter we incur the risk of leaving 
unsound bone, or bone incapable of maintaining its own nutrition, in 
contact with the sinus wall. This, as a rule, is all that is required to bring 
about repair. 

As soon as w 7 e are convinced that the interior of the sinus has become 
infected, there should be no hesitation or unnecessary delay in operating 
upon the sinus itself. 

Indications for Sinus Operation .—The indications for opening the sinus 
are any conditions pointing wdth reasonable certainty to the presence of 
an infected clot. These, in the order of their importance, are: 

(1) Mastoid disease plus symptoms of periodic septic absorption. 

(2) Mastoid suppuration plus streptococcaemia. 

(3) Changes in the sinus wall obviously gangrenous in character; only 
in exceptional cases, however, can the macroscopic evidences of disease be 
relied upon as evidence of intra-sinus infection. 

I know that the views here expressed as to the limited value of mac¬ 
roscopic changes in the sinus w 7 all as indicating intra-sinus infection will 
not have the support of some distinguished aural surgeons. The point 
in regard to which absolute unanimity of opinion may be assumed will 
usually not repay discussion. Those who advocate surgical intervention 
in cases of suspected sinus thrombosis in advance of symptoms of septic 
absorption, do so upon the hypothesis that the appearance of symptoms 
may express rather an advanced stage of the disease,—a stage in some 
cases too late for successful operative intervention. That symptoms of 
sepsis usually indicate clot disintegration is probably true; but that the 
beginning of clot disintegration represents in any considerable percentage 
of cases a stage in which the chance of successful intervention is materially 
reduced, I do not believe to be a fact. 

The laboratory investigations of Dr. Libman, corroborated and checked 
by the clinical studies of Dr. Gruening, have brought out a fact of enor¬ 
mous clinical importance in the study of this disease,—viz., the very rapid 
disappearance of bacteria from the blood after resection of the jugular 


356 INTRACRANIAL LESIONS OF OTITIC ORIGIN 

vein. In most of their cases, the bacteremia was definitely checked 
within 24 to 48 hours after the ligation. In the light of this fact, it seems 
to the writer that we are more than ever justified in a reasonable delay m 
opening the sinus,— i.e., until symptoms of systemic infection shall have 

demonstrated its necessity. 

The accompanying illustration (Pig. 192) gives a clear and correct, 



Lateral sinus 


Circular sinus 
Cavernous sinus 
Transverse sinus 
Inferior petrosal 
sinus 


Superior petrosal 
sinus 

Sigmoid sinus 


Straight sinus 

Torcular 

herophili 


Fig. 192. —Venous channels of the brain. 


though somewhat diagrammatic, picture of the large venous channels of 
the brain, and shows the relation, direct or indirect, between the sigmoid 
sinus and all the others. 

Rationale of Operative Treatment .—The surgical treatment of infective 
sinus thrombosis has represented a gradual evolution, the successive 
stages of which may be traced in the following operations: 

1. Removal of Clot .—The first operations were based upon the hypoth¬ 
esis that the clot itself was the chief source of systemic infection and that 
its removal would end the disease. The operation consisted in opening 




















ABSCESS OF THE BRAIN: ETIOLOGY 


q xiy 

OD i 


the sigmoid sinus and examining its interior for the presence of an organized 
clot. The clot if found was removed. Sterile gauze was then placed 
against the wound in the sinus wall, which was allowed to heal. Its lumen 
was not obliterated. This operation resulted in a slight reduction of the 
mortality, but naturally failed in the great majority of cases. 

2. Removal of Clot and of the Diseased Sinus Wall. —The disappointing 
results following the operation just described soon led to a recognition of 
its comparative uselessness so long as the diseased sinus wall was allowed 
to remain. The scope of the operation was therefore enlarged to include 
removal both of the clot and of the outer sinus wall throughout the extent 
of the incision,— i.e., usually over a considerable portion of the vertical 
limb. This necessitated compression of the sinus above and below, and 
firm packing with sterile gauze of the intermediate portion, thus obliterat¬ 
ing its lumen at the site of the operation. The results of this operation, 
while vastly better than those of that first described, yet failed to control 
the infection in a large percentage of cases. 

3. Removal of Clot and Diseased Sinus Wall plus Ligation of Jugular 
Vein. —The latter operation marked the recognition of the rather frequent 
spread of the lesion from the sigmoid sinus to the jugular bulb or jugular 
vein below. It had become clear, that, for cases in which the limitation 
of the infective process to the sigmoid sinus could not be determined, the 
only treatment offering reasonable protection against further systemic 
poisoning would be one which not only attacks the initial lesion within 
the sinus, but also cuts off the connection of this vessel with the general 
blood stream by ligation or exsection of the jugular. The adoption of 
the jugular operation as part of the surgical treatment of intra-sinus 
infection has enormously reduced the mortality of the disease. Formerly 
regarded as among the nearly hopeless lesions, it is now looked upon 
as a disease in which the prognosis under skilful surgical treatment is 
fairly good. 

The operations upon the sinus and upon the jugular vein will be de¬ 
scribed in detail in a later chapter. 

♦ 

ABSCESS OF THE BRAIN. 

Etiology. —Etiologicallv we are concerned here with only one class 
of cases,—viz., those secondary to middle-ear or mastoid disease. While 
brain abscess may result from either acute or chronic suppurative otitis 
media, all investigations prove that the great majority of cases are due to 
the chronic form of the disease. Thus, Okada, 12 in a series of 145 recorded 
cases, found that 117, or 81 per cent., were due to chronic, while 28 cases, 
or 19 per cent., were caused by acute suppurative disease of the tympanum 
or mastoid. NeumamTs 13 percentages, based upon an investigation of 
151 cases, gave 88 per cent, as due to chronic and 12 per cent, as due to 

12 Okada: Klin. Vortr. aus d. Geb. der Otologie, etc., 3, p. 339. 

13 Neumann: Cerebellar Abscess, Eng. edition, p. 3. 






358 


INTRACRANIAL LESIONS OF OTITIC ORIGIN 


acute disease. In Grunert’s series 14 91 per cent, resulted from chronic and 
9 per cent, from acute tympanic or mastoid suppuration. 

In line with the above are Jansen’s statistics 13 compiled from the rec¬ 
ords of the Berlin Ear Clinic, in which 6 cases of brain abscess occurred in 
2500 cases of chronic middle-ear suppuration, or 1 in 417, and only 1 in 
2650 cases of acute suppurative otitis media. 

Age .—All authorities agree that the great majority of victims are found 
in people between the ages of 10 and 30 years. 

Sex .—Men are more frequent sufferers than women. Thus, of 204 
cases collected by Korner, 16 136 were men and 68 women. Of 188 cases 
collected by Neumann, 17 127 were men and 61 were women. 

Location .—The most frequent sites of brain abscess of otitic origin are 
the temporosphenoidal lobe and the cerebellum, the cerebral far outnum¬ 
bering the cerebellar lesions. The relative frequency with which these two 
regions are attacked is perhaps best indicated in the following citations: 
Barr 1 * in an analysis of 75 cases found the abscess to be in the temporal 
lobe in 55, in the cerebellum in 13, in both cerebrum and cerebellum ( i.e ., 
two abscesses) in 4, in the pons in 2, and in the crus cerebri in 1. 

Leaving out of our consideration abscesses in the rarer situations,— 
e.g., in crus cerebri or pons,—and considering only those of the cerebrum 
and cerebellum, we have the following figures: 



Total number 
of cases. 

Temporal lobe. 

Cerebellum. 

Barr 18 .:. 

68 

55 (81 per cent.) 

79 (67 “ “ ) 

395 (68 “ “ ) 

65 (65 “ “ ) 

336 (63 “ “ ) 

13 (19 per cent.) 

40 (33 “ “ ) 

186 (32 “ “ ) 

35 (35 “ “ ) 

196 (37 “ “ ) 

Korner 19 . 

119 

Heimann 20 . 

581 

H. Tod 21 . 

100 

Neumann 22 . 

532 



In the above citation of Heimann’s interesting statistics the total 
number, given here as 581, includes only cases in which a single abscess, 
situated either in temporal lobe or cerebellum, was present. In Heimann’s 
paper the total number is increased to 645 by the inclusion of many cases 
in which double lesions— i.e., abscesses in different parts of the brain— 
were present. 

Brain abscesses, either cerebral or cerebellar, are usually single, but 
may be multiple. Abscesses may also coexist in the middle and posterior 


14 Grunert: Schwartze’s Handbuch f. Ohrenheilk., Bd. ii, p. 849. 

15 Jansen: Berliner klinische Wochenschrift, 49, p. 1162. 

16 Korner: Die Otitischen Erkrankungen des Hirns, etc., 1896, p. 5. 

17 Neumann: ibid., p. 1. 

18 Barr: Diseases of the Ear, p. 288. 

19 Korner: Die Otitischen Erkrankungen des Hirns, etc., 1896, p. 103. 
20 Heimann: Arch. f. Ohrenheilk., 66, p. 257. 

21 H. Tod: Diseases of the Ear, p. 259. 

22 Neumann: Cerebellar Abscess, Eng. edition, p. 1. 


















ABSCESS OF THE BRAIN: ETIOLOGY 


359 


fossse,— i.e., in the temporal lobe and cerebellum. Thus, in a series of 100 
cases collected by Korner, coincident abscesses of the cerebrum and cere¬ 
bellum were present in 6. In Hunter Tod’s series of 100 cases from the 
records of the London Hospital the double lesion occurred 5 times, while 
Heimann in 645 cases found coincident temporal lobe and cerebellar 
abscesses only 10 times. 

Bacteria .—The investigations of Leutert, Suepfle, Hasslauer, Libman, 
and others have abundantly demonstrated that the streptococcus more 
frequently attacks the brain during suppurative middle-ear disease than 
does any other one micro-organism. It does not follow, however, that the 
brain may not be in serious danger of invasion by other bacteria. That the 
contrary is the fact is made clear by the bacterial findings in 45 cases of 
brain abscess analyzed by Hasslauer. 23 Eleven of these were cases of 
infection following acute middle-ear suppuration, 34 complicating the 
chronic form of the disease. The following is a partial synopsis of Hass- 
lauer’s statistics: 


Brain Abscesses complicating Acute Middle-ear Suppuration. 


Cases 


Pus yielding streptococci in pure culture. 6 

Pus yielding diplococci in pure culture. 

Pus yielding staphylococci in pure culture. ;••••. . 

Pus yielding streptococci and diplococci (mixed infection). 

Pus yielding streptococci and staphylococci (mixed infection). 

Pus yielding diplococci and staphylococci (mixed infection). 


1 

1 

1 

1 

1 

11 


Brain Abscesses complicating Chronic Middle-ear Suppuration. 


Cases 


Pus yielding 
Pus yielding 
Pus yielding 
Pus yielding 
Pus yielding 
Pus yielding 
Pus yielding 
Pus yielding 
Pus yielding 
Pus yielding 
Pus yielding 
Pus yielding 
Pus yielding 
Pus yielding 
Pus yielding 
Pus yielding 
Pus yielding 
Pus yielding 
Pus yielding 


streptococci in pure 


culture.19 


streptococci, diplococci, and Gram-negative bacilli. 

streptococci, diplococci, and staphylococci. 

streptococci and bacilli. 

diplococci in pure culture. 

diplococci and bacilli pyocyanei. 

diplococci, streptococci, and b. proteus. 

diplococci and bacterium coli commune. 

diplococci and Gram-negative bacilli. 

diplococci and Gram-positive bacilli. 

staphylococci in pure culture. 2 

bacillus pyocyaneus in pure culture. 1 

typhoid bacillus in pure culture. 

tubercle bacillus in pure culture. 

pseudodiphtheria bacillus in pure culture. 

bacillus proteus in pure culture. 

bacterium coli commune and cocci. 2 

anaerobic bacilli in pure culture. ^ 

anaerobic bacilli and streptococci. 

34 


23 Hasslauer: Die Mikrooganismen bei den endokraniellen otogenen Komplika- 

iionen, Internat. Zentralbl. f. Ohrenheilk., Bd. v., Heft. I, pp. 15-16. 





























360 


INTRACRANIAL LESIONS OF OTITIC ORIGIN 


Considering together the cases caused by acute and chronic middle 
ear or mastoid suppuration, we have the following results: 

Cases 


Streptococci, in pure culture.,.16 

Diplococci, in pure culture. 2 

Staphylococci, in pure culture. 3 

Bacilli pyocyanei, in pure culture. 1 

Typhoid bacilli, in pure culture. 1 

Tubercle bacilli, in pure culture.. 1 

B. proteus, in pure culture. 1 


Mixed infections 


25 

20 


45 

An analysis of the above demonstrates clearly the following facts,— 
viz.: (1) That a very large proportion of all cases of brain abscess (in this 
series 16 out of 45, or 35per cent.) are due to a pure streptococcus infec¬ 
tion. (2) There is no micro-organism capable of causing purulent otitis 
media which may not also give rise to brain abscess. (3) That in acute 
suppurative disease of the middle ear or mastoid there is greater danger 
of brain abscess in those cases depending upon a pure, or unmixed, infection 
than in those due to a mixed infection. Thus, of the 11 cases in this series 
6 were due to an infection yielding streptococci in pure culture, 1 each to 
an unmixed diplococcus and staphylococcus infection, and only 3 to mixed 
infections. (4) Of cases of brain abscess secondary to chronic middle-ear 
suppuration the percentage of cases showing mixed infections is naturally 
much greater,— e.g., 15 in 34 cases in Hasslauer’s series. This does not 
signify that the average virulence of mixed infections is greater in chronic 
suppurative otitis media, but simply that the relative and actual frequency 
of mixed infections is greater; hence the greater number of brain abscesses 
from which more than one micro-organism may be obtained. 

The above facts are for the most part in accord with the results ob¬ 
tained by other investigators. But, while considerable evidence has 
accumulated as to the relative potency of different bacteria in causing 
brain abscess, little is yet known as to certain differences in the character 
of the abscess itself as determined by the character of the invading micro¬ 
organism. 

Neumann 24 believes that there is a distinct antithesis between the 
diplococci and certain bacilli,—particularly the Gram-negative anaerobic 
bacilli,—in the different structural changes to which they give rise in the 
brain. According to him, a characteristic property of the diplococci is 
their ability to produce an abundant secretion of fibrin from the blood of 
the brain substance immediately surrounding an inflammatory centre. 
Quickly following their invasion of the brain substance, there occurs, in 

24 Neumann: quoted by Korner, Die Otitischen Erkrankungen des Hirns etc 1908 
pp. 56-57. ’ ’’ ’ 












ABSCESS OF THE BRAIN: PATHOLOGY 


301 


addition to the usual inflammatory reactions about the focus of infection, 
the formation of a more or less thick fibrinous membrane or reticulum, in 
the meshes of which large numbers of polynuclear leucocytes are deposited. 
This fibrinous membrane is gradually increased in thickness, its mechanical 
result being a tough, indurated wall separating the abscess cavity from 
the surrounding normal brain substance. In other words, it is a charac¬ 
teristic property of the diplococci, and to some extent of the cocci generally, 
to induce the formation of a firm and resisting abscess capsule,—a con¬ 
dition obviously influencing the prognosis, favorably when a suitable path¬ 
way for the escape of pus has been provided. So strongly convinced is 
Neumann of this characteristic pathologic influence of the diplococci, 
that he regards their presence in pure culture, or their preponderance, in 
the pus obtained from a brain abscess as strong inferential proof of the 
existence of a well-defined abscess capsule. 

The condition is quite different in cases of brain abscess due to infec¬ 
tion by anaerobic Gram-negative bacilli. Such an abscess, according to 
Neumann, is characterized by the absence of a well-defined limiting wall 
or membrane, the boundarj^ between abscess cavity and surrounding 
normal brain substance consisting chiefly of a layer of necrotic brain 
tissue or crumbling detritus. The pus from such an abscess is always 
markedly offensive, and, if some of the bacilli are isolated and cultivated, 
the same offensive odor is reproduced in the resulting growth. Ordinarily 
these micro-organisms exist as harmless saprophytes in the mouth, reach¬ 
ing the tympanic cavities through the Eustachian canals. Their occasional 
virulence in the ear and brain has not been explained. When either dip¬ 
lococci or Gram-negative bacilli are mixed with other bacteria, the control¬ 
ling influence will depend upon the preponderance—either in numbers or 
in degree of virulence—of one or the other. 

Pathology. —In a majority of cases the abscess is situated not far 
from the diseased area of bone forming the immediate gateway of intra¬ 
cranial infection. In others, constituting a decided minority, a consider¬ 
able distance intervenes between the osseous lesion and the resulting 

abscess. 

As to the process by which the infection reaches the interior of the 
brain, two modes of attack have been observed, viz.: 

1. As a result of inflammatory changes in the tympanic or antral roof, 
—with or without perforation,—pus collects between the dura and bone 
in the mid-cranial fossa at a point corresponding to the necrotic area 
(extradural abscess). The dura, being in constant contact with pus, 
undergoes inflammatory changes, at first involving only its outer surface 
but later its entire thickness. Surgical evacuation of the pus not being 
provided, the inflamed dura undergoes necrosis at some point, thereby 
establishing a direct pathway of infection to the pia, and thence to the 
contiguous cerebral structure. This is probably the usual mode of infec¬ 
tion in cases of cerebral abscess complicating acute tympanic or mastoid 

disease. 



362 


INTRACE AXIAL LESIONS OF OTITIC ORIGIN 


2. Without the intermediate formation of an extradural abscess, a 
beginning erosion in the bony plate covering the tympanic vault and 
antrum (tegmen tympani et antri) gives rise to inflammatory changes in 
the adjacent dura, the diseased dura and bone becoming adherent. The 
next stage of this process, according to Macewen, 25 is pronounced thick¬ 
ening of the dura with the formation of granulations upon its inner or 

cerebral surface. This results in a some¬ 
what cone-shaped elevation (Fig. 193), 
which projects into and infects the pia mater. 
Throughout this raised area the necrotic 
bone, the meninges, and superimposed layer 
of brain matter are welded together by the 
products of inflammation. Lateral extension 
of this process being retarded by outlying 
inflammatory adhesions, the pathway of 
infection is toward the interior of the brain. 
Ltus invasion may occur in three ways,—viz., (a) the blood-vessels and 
lymphatics of the pia may carry the infection to the adjacent brain struc¬ 
ture, giving rise to a superficial abscess in close proximity to the area of 
osseous necrosis; (b) branches of the cerebral arteries, being for the most 
part terminal vessels with few anastomotic connections (Macewen), may 
become infected and lead to the formation of an abscess more deeply 
seated within the substance of the brain; or (c) disintegration at the centre 
of the inflamed area may provide a direct pathway for the passage of pus 
from the mastoid to the interior of the brain. 

4n abscess of the brain may vary in size from that of a pea to one 
measured by almost total displacement or destruction of the lobe in which 
it originated. This variation in size explains to some extent the varying 
clinical phenomena exhibited in different cases, and also the fact that an 
abscess may exist for a considerable period while producing absolutely no 
symptoms upon which a diagnosis could possibly be based. 

It is now an accepted fact that brain abscesses differ histopatholog- 
ically in accordance with the presence or absence of a limiting membrane 
or capsule. There are undoubtedly cases in which there is no apparent 
effort at encapsulation, the abscess focus being separated from the sur¬ 
rounding brain structure only by a thin layer of necrotic cerebral tissue 
(Neumann). More often, however, the suppurative invasion of the brain 
is followed by a productive or hyperplastic inflammation in the surround¬ 
ing brain tissue, as a result of which a protective wall or capsule is gradually 
formed (Macewen, R. Muller). While such a wall or capsule undoubtedly 
dela} s the progress of the disease toward a fatal ending, the proportion of 
cases in which spontaneous healing through resorption and cicatrization 
occurs is probably exceedingly small. 

Symptoms.— Considering the symptoms as they may occur from the 



Fig. 193. —Invasion of brain through 
tympanic vault. (After Macewen.) 


25 Macewen: Pyogenic Diseases of the Brain, etc., pp. 71-72. 










































































ABSCESS OF THE BRAIY: SYMPTOMS 


363 


inception of the abscess to its successful evacuation or to the fatal ending, 
they may be divided into the following groups roughly typifying the stages 
of the disease,— e.g., (1) those of the initial stage (onset), or stage of in¬ 
vasion; (2) those of the formative stage, or stage of gradual increase in 
intracranial pressure; (3) those of the latent stage, or stage of encapsula¬ 
tion; and (4) those of the terminal stage, corresponding to the final ex¬ 
haustion of the patient through septic absorption, or to the rupture of 
the abscess into ventricle or subarachnoid space. 

Initial Stage, or Stage of Invasion. —It is reasonable to suppose that 
breaking down of the anatomical barriers between the extradural and 
subarachnoid spaces — or, in other words, the sudden extension of the 
suppurative process to the pia mater f —should give rise to definite 
symptoms. Macewen states that this stage of brain abscess formation 
is almost invariably announced by a chill, or rigor, and always by high 
temperature and severe headache. Vomiting, with or without nausea, 
is usually, but not invariably, present. These symptoms may be due 
to the initial changes at the site of the forming abscess cavity, but 
to the writer it seems much more probable that they are due solely 
or chiefly to a circumscribed cortical encephalitis surrounding the point 
of attack. Unfortunately, the onset, coming as it most frequently 
does during the course of a chronic suppurative otitis media, repre¬ 
sents a stage which the aurist rarely actually sees. Its diagnostic 
significance may also be obscured by the number of other conditions 
which might cause very similar disturbances. These initial symptoms 
are usually of short duration, the fever and headache subsiding within a 
few days. They may leave the patient for a time in apparently fairly 
good condition, or may be immediately followed by symptoms of 
increased intracranial pressure. 

Second Stage, or Period of Increasing Intracranial Pressure. —Between 
the onset and the development of further symptoms, a period may inter¬ 
vene in which no very characteristic phenomena are present. Following 
this intermediate period of quiescence, or in some cases crowding closely 
upon the onset, the first symptoms betokening the fully formed abscess 
are usually in some degree referable to increased intracranial pressure. 

In order to take up the phenomena of the second stage in some regular 
order, it may be best to group them under three heads,—viz., (a) general 
symptoms of intracranial disturbance or compression, (b) symptoms due 

to septic absorption, and (c) focal symptoms. 

The general symptoms of intracranial disturbance or compression in¬ 
clude headache, restlessness and insomnia, temperature and pulse changes, 
mental lethargy or obscuration, inability to exert muscular force, changes 
in the eye grounds, gradually increasing somnolence. 

Headache. —The headache of the second stage of brain abscess differs 
from that of the onset, or from that of acute leptomeningitis, in that it 
is not usually of the excruciating type which causes the patient to cry 
out. It has in typical cases rather the character of a dull, boring ache. It 


364 


INTRACRANIAL LESIONS OF OTITIC ORIGIN 


has also this characteristic,— i.e., that, while more or less constant, or at 
least very persistently recurrent, there is a tendency for its severity to be 
reduced as the abscess increases in size and the senses become dulled by 
increasing intracranial pressure. It varies considerably in its location in 
different cases, or it may attack at different times different parts of the 
head. Thus, it may be referred to the side of the head corresponding to 
the lesion, to the frontal region, or to the occiput; or it may alternate 
between the frontal and occipital regions. In most cases the headache 
varies in severity at different times, being usually worse at night. During 
the day it may be slight or absent,—or at least may not be complained of, 
—but as night approaches the pain returns or its intensity is increased, 
contributing to the prevention of sleep. With these patients, even 
during the period in which pain is not complained of, there is probably 
a more or less constant sense of cerebral disturbance or compression 
which must be inexpressibly harassing, and which probably contrib¬ 
utes to the restlessness and insomnia which more or less characterize 
the disease. 

Insomnia .—It seems a paradoxical statement that both somnolence 
and insomnia are strongly characteristic features of this disease. The 
patient may be practically sleepless during most of the twenty-four hours 
or, as is more often the case, his sleep is exceedingly fitful, disturbed, and 
easily broken, so that he sleeps and wakes many times within the hour, 
and in the morning is unrefreshed. When severe headache is present, the 
insomnia may of course be ascribed, in part at least, to that symptom. 
But even in cases in which headache is not particularly severe, insomnia 
is usually a prominent symptom. In such cases— i.e., when headache is 
not complained of—the insomnia acquires special diagnostic importance 
from the fact that its degree and particularly its persistence are out of all 
proportion to any causes which can be discovered outside of a possible 
lesion within the skull. A patient who came under the writer’s observation 
some years ago, and who died later from what proved to be the rupture 
of a temporosphenoidal abscess into the ventricles and subarachnoid 
space, described his insomnia somewhat as follows: “Though I am no 
longer able to work, I get very tired while doing nothing. I become not 
only very tired but very sleepy, so that I can hardly keep my eyes open; 
but when I lie down I can not sleep.” 

Temperature .—Following the initial rise described as characteristic 
of the onset, the temperature usually returns to normal or thereabout. 
From this time its variations may be confined within exceedingly narrow 
limits, not at any time rising to more than a point or two above the normal 
line. It is characteristic of a deep-seated brain abscess that the tempera- 
true may remain near the normal line, making occasional slight excursions 
either above or below it. Thus, in a case of suspected intracranial infec¬ 
tion, a temperature curve ranging from a degree below normal to one or 
two degrees above it would be regarded as characteristic of brain abscess. 
On the other hand, in the presence of other reliable signs, a perfectly nor- 



I 


ABSCESS OF THE BRAIN: SYMPTOMS 365 

mal temperature could not be regarded as proof that the abscess was not 
present. Naturally, there are cases of brain abscess, even where no evi¬ 
dences of meningeal inflammation are present, in which the temperature 
either runs a higher course or makes occasional excursions to a higher level. 

In cases presenting other conclusive evidences of brain abscess the 
presence or absence of fever would lead — so far as they might have 
any significance — to the following inferences: With complete absence 
of fever one would expect to find a rather deep-seated abscess, 
whereas persistent fever would point — in the absence of meningitis 
to cortical irritation, and therefore to a lesion in close proximity to the 
cerebral cortex. 

Presumably the occasional excursions below the normal point are due 
to pressure transmitted to some centre having to do with temperature con¬ 
trol, the excursions in the opposite direction being the usual reaction to 
pus accumulation wherever it may be found in the body. 

Pulse Changes .—With the gradual increase in intracranial pressure 
is frequently noted the characteristic slowing of the pulse-rate. The pulse, 
which under normal conditions has perhaps recorded 80 or 85 beats per 
minute, is gradually reduced to 75, 70, 60, 50, or perhaps 40 beats to the 
minute. This phenomenon is usually regarded as a result of increased 
pressure, the gradual reduction in pulse rapidity progressing with the grad¬ 
ual increase in the size of the abscess. On the other hand, quite marked 
pulse retardation has been observed in certain cases in which operation 
has given exit only to a very small amount of pus, and also in others ending 
fatally in which the autopsy has brought to light only a small abscess 
cavity. Probably the view held both by Macewen and Gowers—viz., 
that this symptom is due in some cases simply to irritation of some centre 
having an inhibitory influence over the heart action is to be taken into 

account in explaining these differences. 

When the abscess is successfully evacuated, the slow pulse-rate is 
usually promptly corrected, going first somewhat above normal e.g., 110 
or 120 per minute—and then receding gradually to the normal line 

(Macewen). 

Mental Dulness— With increase in cerebral pressure, and depending 
therefore somewhat upon the size of the abscess, certain defects of cere¬ 
bration usually make their appearance. The most characteristic mental 
change is one of mental lethargy. Even with unmistakable evidences of 
cerebral pressure, the patient is not exactly unintelligent, but may be 
decidedly dull mentally. In such cases, cerebration, though not ablated, 
is slow, ‘difficult, and may be distinctly retarded. Thus, when asked a 
simple question, the answer, though correct, is given after an appreciable 
pause as though its interpretation had required considerable ehort. lhis 
retardation is sometimes so pronounced as to lead the physician to con¬ 
clude that his question has not been heard. After he has ceased to expect 
a reply, however, the answer is given, and given correctly, showing that 
cerebration is obscured or impeded, but not otherwise disturbed. With 


366 


INTRACRANIAL LESIONS OF OTITIC ORIGIN 


this condition the patient is often extremely drowsy, falling often into 
fitful sleep, from which he is easily aroused, but into which he quickly 
relapses when left undisturbed. Even more characteristic of a large 
temporosphenoidal abscess is the failure in the power of sustained atten¬ 
tion. While the patient may be able to answer any simple question cor¬ 
rectly, it may be quite impossible for him to concentrate his attention on 
any subject for more than a few minutes. For this reason it may be im¬ 
possible for him to perceive the meaning of any but the simplest questions; 
or, having something to communicate, he may begin to speak and lose his 
train of thought while speaking; or, again, he may call for something to be 
brought to him, and altogether forget his request before it can be brought. 
Naturally, with mental processes depending upon such shallow and in¬ 
secure impressions, they are not likely to be recalled after the patient 
recovers. 

A striking example of the depression or obstruction without actual 
ablation of the mental functions is found in a case reported by Macewen 26 
in which the patient recovered after evacuation of a large temporosphe¬ 
noidal abscess. On the day of admission to hospital, he was able in reply 
to direct questions to give intelligent and correct replies as to his address, 
occupation, history of attack, his subjective symptoms, etc. On the day 
following evacuation of the abscess, however, he awoke without the slight¬ 
est memory of the events of the previous day,— i.e., “he realized for the 
first time that he was in a place unknown to him, and had no idea how he 
came to be in it.” 

Loss of Motor Will Power .—With gradual loss of the power of sus¬ 
tained attention, there is always an increasing tendency toward drowsiness. 
The condition is one of mental and physical lethargy and indifference. 
The patient can not be stimulated to the exercise of any sustained effort, 
either mental or physical. While paralytic disturbances may be com¬ 
pletely absent, he presents in advanced stages of the disease an ap¬ 
pearance of marked physical weakness, which is due not to actual loss 
of muscular force, but to loss of the potential will power necessary to call 
it into activity. 

Eye-ground Changes .—Changes in the eye-grounds— e.g., papillitis, 
optic neuritis—may occur with any intracranial disease causing increased 
pressure. They may be present, therefore, in cases of brain tumor, brain 
abscess, or with meningitis. 

Urbantschitsch 27 cites the work of E. and 0. Ruttin, who made sys¬ 
tematic examination of the eye-grounds in a large number of intracranial 
lesions coming under observation in the Urbantschitsch clinic and hospital 
service in Vienna. According to these investigators, the eye-grounds 
were found normal in all cases of otitic abscess of the temporal lobe; they 
were normal in the majority of cases of cerebellar abscess, whereas in 


26 Macewen: Pyogenic Diseases of the Brain, etc., pp. 155-161. 

27 Urbantschitsch: Lehrbuch d. Ohrenheilk., p. 514. 




ABSCESS OF THE BRAIN: SYMPTOMS 


36 ? 


advanced otitic meningitis optic neuritis was commonly present. Argu¬ 
ing from these premises they concluded that a positive finding of papil¬ 
litis or optic neuritis in a case of suspected intracranial involvement is to 
be regarded as pointing strongly away from otitic cerebral abscess as the 
lesion present. Interesting as these observations may be, eye-ground 
changes resulting from brain abscess have been too frequently recorded 
to warrant so sweeping a deduction without further investigation. 

So far as we are justified in any positive statement, the consensus of 
opinion is probably about as follows: Eye-ground changes (papillitis, 
choked disk, optic neuritis) occur much more frequently as a result of 
slow-growing brain tumors than with brain abscess. They also occur 
more frequently with meningitis than with brain abscess. They do, 
however, result from brain abscess in certain cases. 

Papillitis is more frequently seen in brain abscess than is optic neuri¬ 
tis, for the reason that the rapid course of a cerebral abscess either to a 
fatal termination or to recovery through operation often does not allow 
time for the development of a well-marked neuritis. When present, optic 
neuritis is usually a late sign, coming only when the abscess has reached 
considerable size and produced very marked increase of intracranial 
pressure. 

Macewen 28 states that optic neuritis occurs “neither in cases of 
cerebral abscess which have run a rapid course, the period for its 
production being too short, nor where the cerebral abscess is small 
and the degree of surrounding inflammatory reaction is slight.” If 
this be true, the association of optic neuritis with other well-marked 
symptoms of brain abscess should be of favorable import to this extent, 
—viz., that it would seem to point to a slowly developing abscess 
of considerable size, and one having presumably a well-formed capsule. 
Such an abscess should offer favorable conditions for successful surgical 
evacuation. 

Papillitis or optic neuritis may occur in one or both eyes, and may be 
confined to either eye. That is to say, an abscess in the right temporal 
lobe may give rise to fundus changes in the left eye, or vice versa. They are 
in no sense, therefore, focal or localizing symptoms. 

To epitomize: Changes in the eye-grounds usually mean somewhat 
prolonged increase of intracranial pressure. Associated with other symp¬ 
toms of brain abscess, they are undoubtedly an aid to diagnosis. Abso¬ 
lutely normal eye-grounds do not, however, constitute a disproof of such 
a lesion. 

Vomiting, which is spoken of in most text-books as an occasional 
symptom of cerebral abscess, is undoubtedly a common feature of the 
onset. After the initial stage is past, vomiting is comparatively rare. 
As a late symptom it is a much more frequent accompaniment of cere¬ 
bellar abscess than of abscess of temporal lobe. Occurring late in temporo- 


28 Macewen: Pyogenic Diseases of the Brain, etc., p. 141. 





368 


INTRACRANIAL LESIONS OF OTITIC ORIGIN 


sphenoidal abscess, it would suggest at least the possibility of meningeal 
involvement. 

Symptoms of Sepsis .—The symptoms of sepsis in this disease differ 
somewhat from those which betoken septic absorption from suppurative 
lesions in other parts of the body. The temperature curve, for example, 
usually does not show the wide fluctuations commonly associated with 
septic absorption; on the contrary, its excursions are usually confined be¬ 
tween narrow limits, and it may remain during considerable periods prac¬ 
tically normal. As offsetting this paradoxical absence of fever, there are 
two conditions which probably in many cases have to do with the septic 
condition of the patient,—viz. : 

1. There is a progressive, and in some cases remarkably rapid, loss of 
flesh and strength, which no lesion of otitic origin short of intracranial 
infection could possibly give rise to. Meningitis being excluded, the rapid 
progression of this change, watched and measured from day to day, may 
of itself constitute a strong indication of cerebral abscess. 

2. Another feature which is not easily described in exact or scientific 
terms, but which is sometimes most striking, is the early disproportionate 
appearance of grave illness as compared with any other symptoms present. 
This contrast is in some cases so striking as to suggest at once an intra¬ 
cranial complication. 

Probably these changes in the weight, strength, and general tone are 
due in part to disturbance of certain centres having to do with tissue 
metabolism, and in part to the peculiar potency of septic agents absorbed 
through the structures of the brain. That they are not to be regarded 
altogether as trophic changes due to compression, seems deducible from 
their absence in certain cases of encapsulated abscess of considerable 
size,—so-called ambulatory cases,-—in which the patient’s condition is 
fairly well maintained until shortly before the terminal stage is reached. 

Focal Symptoms .—Under this heading we may for convenience include 
any clinical change, subjective or objective, which throws light upon the 
site of the lesion. 

Muscular Paresis .—In large temporal lobe abscesses, even when there 
are no phenomena which indicate the particular gyri involved, there is apt 
to be a slight contralateral paresis of the upper extremity. This paresis 
may be so slight as to escape notice unless carefully looked for. On the 
other hand, a careful observer may note a comparative languor, or effort, 
in the movements of the hand and arm opposite to the lesion as compared 
to its fellow. The best means of determining this unilateral deterioration 
in muscular power is by comparing the grip of the two hands, either by 
requiring the patient to squeeze the examiner’s hand, first with one hand 
and then the other, or, better still, by means of a dynamometer. The pa¬ 
resis of the hand and arm is noticeably present in many cases in which no 
loss of power in the lower limb can be determined. The relative frequency 
of this involvement of the upper extremity and the comparative immunity 
of the lower, is made clear when we consider the relation of an abscess in the 


ABSCESS OF THE BRAIN: SYMPTOMS 


369 


temporosphenoidal lobe to the motor area above it; for, if we regard this 
paresis as resulting wholly from transmitted pressure, it becomes evident 
that this pressure will in a majority of cases be exerted chiefly upon the 
motor area of the face, shoulder, 
arm, and hand, and only slightly 
or not at all upon that of the leg 
or foot (Fig. 194). 

Muscular Spasms .— Muscular 
contractions are by several auth¬ 
ors mentioned as among the occa¬ 
sional symptoms of brain abscess. 

They can occur as a result of 
such a lesion only when, directly 
or indirectly, the motor area is irri¬ 
tated. A large and rapidly formed 
abscess in the temporal lobe might 
induce localized convulsions by 
rapidly developed pressure upon 
the lower part of the precentral 
lobe, but the effect of such pres- u P° n motor area above, 
sure is much more likely to be the 

reverse,— i.e., in the direction of paresis or paralysis of the muscle groups 
involved. A class of cases in which muscular contractions would be more 
likely to occur are those described by Neumann in which there is little 
or no tendency to the formation of a limiting capsule. This absence of 
a limiting membrane might result in a surrounding encephalitis which 
might easily extend cortically from the temporal lobe to the motor area 
of the frontal. Definite muscular spasms are exceedingly rare as a 
symptom of temporosphenoidal abscess. Should they occur without symp¬ 
toms of meningeal involvement, they would, of course, have some value 
as throwing light upon the position and particularly upon the size of the 
abscess, or as betokening an accompanying and extending encephalitis. 

Localized Paralyses .—The theory of contralateral paralysis as a result 
of cortical brain lesions is so universally understood as hardly to require 
mention in a modern text-book. From the usual position of otitic abscess, 
— i.e., in the temporosphenoidal lobe,—monoplegias are rarely seen. If 
they did occur they would suggest an extension of the suppurative process 
from one lobe to another, as it is hardly conceivable that the influence of 
pressure transmitted from the temporal lobe to the precentral cortex 
should be limited to the motor area of a single muscle, or to its closely 
related group. A true monoplegia would, therefore, suggest very strongly 
the possibility of a secondary abscess. 

More or less widespread paralysis is an occasional phenomenon of 
otitic brain abscess, and may result either from transmitted pressure 
upon the cortical motor area or from direct involvement of the internal 
capsule. As to which type of lesion exists in a given case, we may take 
24 



Fig. 194. — (Diagrammatic.) Vertical cross sec¬ 
tion of brain, showing influence of transmitted pres¬ 
sure from temporosphenoidal abscess (shaded area) 












370 


INTRACRANIAL LESIONS OF OTITIC ORIGIN 


into consideration the following conditions, shown diagrammatically in 
Figs. 195 and 195a: (1) A temporosphenoidal abscess capable of producing 
widespread paralysis by pressure upon the motor cortex would necessarily 
be of a very considerable size; it would be likely therefore to produce 
other manifestations of increased pressure ( e.g ., mental dulness or obscura¬ 
tion, slow pulse, and possibly, in a left-sided lesion, some form of aphasia). 



Fig. 195.—(Diagrammatic.) Vertical cross Fig. 195a. —(Diagrammatic.) Vertical cross 

section of brain, showing a large temporosphe- section of brain, showing small abscess (shaded 
noidal abscess (shaded area). area) involving internal capsule. 


From the anatomical relation of the temporal lobe to the ascending frontal 
lobe, it is clear that pressure would be exerted most forcibly upon the lower 
third (face, arm, etc.) and least on the upper third (foot, leg). This is 
shown by Fig. 195. (2) An otitic abscess of comparatively small size 

involving the internal capsule would be (a) more likely to produce wide¬ 
spread hemiplegia, and (b) less likely to give rise to other pronounced 
pressure symptoms (Fig. 195a). 

The presence, therefore, of contralateral paralysis, pronounced in face, 
arm, and hand, but slight or absent in the lower limb; markedly slow 
pulse; pronounced mental dulness, drowsiness, etc., would suggest the 
results of pressure from a large temporosphenoidal abscess. On the other 
hand, a widespread paralysis or even paresis,— i.e., involving the leg and 
foot equally with the upper extremity,—particularly if other pressure 
symptoms were absent or inconspicuous, would point to a lesion involving 
the internal capsule. 

A form of paralysis which has been repeatedly described as resulting 
from brain abscess is that in which a contralateral hemiplegia coexists 
with motor oculi paralysis (ptosis, external squint, inability to rotate the 
eye in other directions) on the side corresponding to the lesion. This may 
be produced in two ways,— i.e., by a lesion involving the crus cerebri 
(explained on pages 329-330), and by a large temporosphenoidal abscess 
exerting pressure at once upon the cortical motor area and on the third 
nerve. Macewen has described two such cases resulting from direct pres- 




















ABSCESS OF THE BRAIN: SYMPTOMS 


371 


sure upon the motor cortex, and he gives the following differential points 
between the two lesions: When the contralateral paralysis is the result of 
pressure transmitted to the cortical motor area, the foot and leg, from the 
position of their motor centre, escape wholly or are only slightly involved. 
When caused by a lesion of the crus cerebri, the hemiplegia is usually 
widespread,— i.e ., involves equally the upper and lower limbs. 

Pupillary changes may or may not be present in cases of temporo- 
sphenoidal abscess, depending, no doubt, on the location or size, and the 
consequent disturbance of pressure. When present, they differ from 
changes in the fundus oculi in that, while the latter may involve either eye, 
or both, pupillary changes occur, as a rule, only in the eye corresponding 
to the side of the brain in which the abscess is located. It is, therefore, to 
some extent a focal symptom. The pupil may be either contracted or 
dilated, or, beginning with contraction, may end—as the abscess increases 
in size and intracranial pressure is augmented—in stable mydriasis (Mac- 
ewen). In some cases in which the pupils are apparently of equal size, a 
useful and interesting sign of abnormal unilateral pressure may be found in 
the sluggish pupillary reaction of the eye corresponding to the side of the 
lesion, which responds slowly to accommodation and light. In such a case 
one would expect stable inequalities of pupillary contraction to develop 
later, unless of course the abscess were evacuated by surgical means. 

Aphasia. —The various cortical centres in which are stored the memory 
pictures, or impressions, essential to coherent speech are situated in the 
left side of the brain in right-handed persons and in the right hemisphere 
in left-handed persons. Aphasia may be looked for, therefore, only in 
cases of suspected disease in the side of the brain in which these centres 
are known to be,— i.e., the left brain in a right-handed individual, and 
vice versa . 

Note. —As the subject of aphasia is a most important one and one to which very- 
limited space can here be given, the student is referred to Chapter XII, in which will 
be found a chart of the more important memory centres concerned in speech, with a 
brief discussion of their functions and the various speech defects following their injury 
or destruction. 

Sensory Aphasia. —The commonest speech defect in otitic abscess is 
the form of sensory aphasia known as word-deafness. Its presence is deter¬ 
mined in the following way: The patient is shown some familiar object— 
e.g.y a watch—and is asked to name it. He may be unable to do so, or may 
call it by some name having no relation to a time-recording instrument. 
He is next asked what it is used for, and he answers correctly “to tell the 
time of day with.” We know, therefore, that he recognizes its form, and 
from this its uses. We now ask him the uses of some familiar object which 
is not exposed to his view,— e.g., a saw, a hammer, or a pencil,—and if the 
name awakens no memory of it, but he is able to recognize it as soon as it is 
shown to him, we have a clear example of word-deafness. Now repeating 
our first experiment of showing him a watch,—of which he recognizes the 
uses but can not recall the name,—ask him if it is a knife, a hammer, or a 


372 


INTRACRANIAL LESIONS OF OTITIC ORIGIN 


watch, and he may promptly say that it is a watch. This shows that his 
aphasia is due to a subcortical lesion which has cut off the memory centre 
for sound impressions from association with other memory centres con¬ 
cerned in speech, but that the “centre” itself is not destroyed, and that 
its activity can be temporarily re-established through certain association 
tracts when the object is seen and its name heard simultaneously. It is, 
therefore, a partial word-deafness, as distinguished from the total word- 
deafness which would occur if the cortical centre for sound memories were 

actually destroyed. ... 

Partial word-deafness resulting from a subcortical lesion gives rise to 

the commonest form of sensory aphasia met with in otitic brain abscess, a 
fact which might be expected from the position of the special centre in¬ 
volved,—a position naturally exposed to pressure from a temporosphe- 
noidal abscess (Fig. 187). This form of sensory aphasia may vary some¬ 
what in different cases in accordance with the extent to which the centre 
for sound memories is isolated. Thus we may have: (a) The common 
form, described above, in which the patient, though mentally depressed 
and disinclined to any unnecessary speech, is yet able to communicate his 
wants in short, simple sentences. The partial word-deafness of such a 
patient might be easily overlooked, unless he were subjected to systematic 
tests by the method above described, (b) In cases of more advanced word- 
deafness the loss of memory for word sounds may be so pronounced as to 
be easily noticed in his simplest utterances. Such an example may be 
found in a very interesting case of left temporal lobe abscess reported by 
McKernon, 29 in which the patient in endeavoring to communicate his 
wants would both “mispronounce words and call articles by wrong names.” 
(c) Still another phase of word-deafness is found in the case reported by 
Gehuchten and Goris, 30 in which the patient, a man of 40 years, suffering 
from left temporosphenoidal abscess, had so far lost all sound memories 
that he could not understand the simplest spoken sentence. That the 
disability was due simply to the isolation of the centre for sound memories 
was shown by his ability to understand written communications perfectly 
and to answer all questions intelligently in writing. 

A moment's thought will show that the above differences are apparent 
rather than real, and that they represent only different grades of partial 
word-deafness. A very interesting case of sensory aphasia belonging to the 
same class, and one which well illustrates the fact that the aphasic indi¬ 
vidual may within certain limits think fairly coherently, was recorded by 
Dean, of Iowa. 31 This patient, a man of 35 and an habitual smoker, 
developed an otitic abscess in the left temporal lobe, the symptoms of 
which were temporarily relieved by operation. This man was able to 
recall the symptoms he had experienced before surgical relief was obtained, 

29 McKernon: Report of a Case of Temporosphenoidal Abscess, Annals of Otology, 
May, 1902. 

30 Gehuchten and Goris: Le Nevraxe, vol. iii, p. 65. 

31 Dean: Brain Abscess of Otitic Origin, Annals of Otology, vol. xix, p. 543. 




ABSCESS OF THE BRAIN: SYMPTOMS 


373 


and he defined very clearly the type of aphasia which had been present by 
his account of the suffering he had endured for want of tobacco. He 
wanted to smoke and knew what he wanted, but stated that he had been 
unable to make his wants known, for the reason that he could not command 
any of the words required to indicate tobacco or its uses. 

Psychical blindness (sensory visual aphasia) in pure form is comparatively 
rare as a result of otitic brain abscess. As with word-deafness, the patient 
suffering from psychical blindness is unable to give the name of a familiar 
object shown him. His inability to do so is due, however, not to loss of 
the memory pictures of word sounds, but to a loss of memory for the visual 
impressions of familiar things. He can not, therefore, give the name of a 
hammer, knife, or pencil shown him for the reason that these objects no 
longer appear familiar to him, and, therefore, awaken no memory either 
of their uses or their names. The condition is due to a lesion—usually 
subcortical—which has cut off from association with other centres the 
special memory centre for the visual impressions of things. This centre, 
it will be remembered, is situated in the second occipital convolution (Fig. 
187). The aphasia dependent upon psychical blindness is clinically dis¬ 
tinguishable from that associated with word-deafness by the fact that the 
patient is able to recall the uses and general character of familiar objects 
when their names are called, though he may receive no mental impressions 
from a familiar object seen. 

Word-blindness (causing sensory agraphia) may coexist with psychical 
blindness or may occur independently. It is present when the patient can 
no longer recall or recognize the forms either of individual letters or written 
words. He is, therefore, unable either to read or write (sensory agraphia). 
It is due to a lesion which isolates the centre for the visual memory pic¬ 
tures of written words or symbols, this centre being situated in the angular 
gyrus. 

Motor aphasia is mentioned in many text-books as among the occasional 
symptoms of brain abscess. It would occur with any lesion which de¬ 
stroyed or isolated the memory centre for the motor efforts necessary in 
speaking, this being located in the posterior end of the third frontal convo¬ 
lution, “Broca’s convolution.” As an example of motor aphasia may be 
mentioned Banti’s case 32 in which the patient, while mentally quite 
coherent and understanding everything that was said to him, could not 
utter a single word. Though unable to speak, he had a clear understanding 
both of spoken and written language, and could himself communicate his 
thoughts quite rationally by writing. This case finally ended fatally, 
and the autopsy brought to light “a patch of yellow softening at the pos¬ 
terior end of the third frontal convolution.” 

Many cases of motor aphasia resulting from brain tumor and other 
lesions have been recorded, but I have personally never known of a case 
secondary to otitic brain abscess. Nor will it be found easy to find a well- 


32 Banti: Gordinier, Anatomy of the Central Nervous System, p. 473. 





374 


INTRACRANIAL LESIONS OF OTITIC ORIGIN 


authenticated case recorded in otological literature. It is mentioned 
simply as a possible, but certainly rare, symptom of otitic abscess. 

Motor agraphia (described on page 337) is dependent upon a some¬ 
what analogous condition, involving, however, the centre for the motor 
effort memories involved in writing. According to Gordinier, who de¬ 
scribed a classical case coming under his own observation, 33 this centre is 
situated in the posterior end of the second frontal convolution. It rarely 
or never occurs singly in brain abscess secondary to otitic disease. 

Course of the Disease— Brain abscess, unless relieved by surgical means, 
leads regularly, either through a more or less prolonged latent period 
or more rapidly, to the terminal stage ending in death. Of the latent 
stage, or stage of encapsulation, we know nothing beyond the fact that, 
in certain cases in which death has resulted from other causes, the autopsy 
has revealed either the cicatrices representing small abscesses long since 
absorbed or, more rarely, an encapsulated cyst or abscess which had long 
ceased to cause any characteristic symptoms. Such spontaneous cure or 
prolonged encapsulation without untoward result is probably exceedingly 
rare. 

The Terminal Stage .—In fatal cases death usually comes in one of 
two ways,— i.e.: 

(a) The progressive loss of strength and flesh leads finally to extreme 
emaciation, the patient presenting a mere shadow of his former self. The 
mental apathy or dulness which characterizes the earlier stage is gradually 
deepened into a condition of somnolence from which it is difficult even 
momentarily to arouse him, this in turn giving way to a condition of coma. 
The pulse, which has perhaps been abnormally slow, may become rapid 
and irregular. The respirations, on the other hand, are usually slower, 
sighing, or may become stertorous in character. Death finally results 
from exhaustion. 

(b) In other cases death results from rupture of the abscess into the 
ventricles and subarachnoid space. This may occur only when the patient 
is near death from exhaustion, or it may occur comparatively early in the 
disease. I recall one instance in which an unsuspected abscess ruptured 
while the patient was up and walking about the ward. In either case the 
catastrophe is invariably followed by a characteristic train of symptoms. 
The face assumes a death-like or livid hue. The temperature quickly 
rises to 103° F., or higher, while the pulse-rate, which may have been 
abnormally slow, is increased to 140 or more per minute. The respirations 
become slower, labored, and finally stertorous, as the patient sinks into a 
stuporous condition. The pupils may be inactive and unequally dilated. 
It is obvious that the flooding of the brain surfaces with pus must give rise 
to more or less diffuse suppurative leptomeningitis, this condition being 
largely responsible for the quick termination. Death usually ensues 
within one or two days. 


33 Gordinier: Amer. Journal of Med. Sciences, May, 1899. 





CEREBELLAR ABSCESS: SYMPTOMS 


375 


Prognosis. —Leaving out of our consideration the exceptional in¬ 
stances of spontaneous recovery, it may be said that the usual termination 
of a brain abscess which has not been relieved surgically is death. The 
treatment, therefore, is surgical, and will be described in a later chapter 
dealing with the operative management of otitic brain lesions. 


CEREBELLAR ABSCESS. 

As we have seen from the statistics of various investigators (p. 358), 
cerebellar abscesses constitute about one-third of all otitic brain abscesses. 
Of these, not more than 15 or 20 per cent, are the result of acute tympano¬ 
mastoid disease, the remaining 80 or 85 per cent, being a complication of 
chronic middle-ear suppuration. 

Symptoms. —As with most acute intracranial lesions, the symptoms 
may be considered under two heads,—viz., general symptoms of intra¬ 
cranial disturbance or compression; and focal symptoms ,— i.e ., those which 
point definitely to the cerebellum as the site of the lesion. 

The general symptoms are so nearly identical with those already de¬ 
scribed in connection with temporosphenoidal abscess that they may be 
reviewed very briefly. They include headache, vomiting, temperature and 
pulse changes, rapid emaciation, eye-ground changes, mental dulness, etc. 

The headache in typical cases differs from that of temporosphenoidal 
abscess chiefly in that it is usually more severe, more persistent, and more 
frequently confined to the side of the head and to the regional area of the 
lesion. It may occur as an early symptom or only after the lesion is well 
advanced. Once it has made its appearance, it is usually an exceedingly 
persistent and harassing symptom. Vomiting may or may not be present. 
This fact, however, should be remembered,—viz., that recurrent vomiting 
(i.e., coming at intervals throughout the entire course of the disease) is far 
more common with cerebellar abscess than with abscess of the temporo¬ 
sphenoidal lobe, in which vomiting is exceedingly rare except at the onset. 
In a case coming under the writer’s observation, the two symptoms above 
mentioned— i.e., persistent headache and recurrent vomiting were dur¬ 
ing the greater portion of the attack practically the only symptoms pointing 
to endocranial disease. The temperature and pulse changes are much the 
same as in cerebral abscess. Fever is usually absent or inconspicuous, 
unless the meninges are also involved. A temperature range occasionally 
falling below the normal line is common with cerebellar as with cerebral 
abscess. Bradycardia is said to be a very frequent symptom of cerebellar 
abscess (Neumann); according to my observation and reading of the lit¬ 
erature, it occurs in about one-third of all cases. Changes in the eye- 
grounds —papillitis, choked disk, optic neuritis—are much more frequently 
present in cerebellar than in cerebral abscess (Ruttin, Neumann), and the 
optic neuritis of cerebellar abscess is very frequently of such grade as to 
cause considerable, though not usually permanent, impairment of sight 
(Macewen). Rapid emaciation is a striking feature in many cases of cere- 


376 


INTRACRANIAL LESIONS OF OTITIC ORIGIN 


bellar abscess. Occurring, as it frequently does, in cases in which fever is 
absent or of very moderate grade, it must be explained as a trophic change, 
due probably to compression or disturbance of some centre strongly influ¬ 
encing tissue metabolism. Mental lethargy , dulness, or obscuration is not 
usually present in cerebellar abscesses of moderate size, and when present 
probably always indicates an abscess of sufficient size to have induced 
marked increase in general endocranial pressure. 

Muscular paralysis is a rare symptom of cerebellar abscess. Korner 
has pointed out that transmission of pressure from a cerebellar abscess to 
the cortical motor areas would be strongly resisted by the tentorium except 
in the case of very large abscesses. On the other hand, muscular paralysis 
or paresis might easily result from compression of the pons or medulla by a 
cerebellar abscess of comparatively small size. Such paralyses have been 
observed, sometimes contralateral and in other cases on the same side as 
the lesion. Macewen 34 explains these differences as corresponding to the 
level at which the motor tract is compressed. He points out that the cere¬ 
bellum passes to some extent into the foramen magnum, and may extend 
further under abnormal pressure. On this hypothesis, he explains the 
occasional contralateral paralyses as due to pressure upon the pons, and 
the otherwise confusing paralyses on the side of the lesion as due to pres¬ 
sure upon the medulla at a level below the crossing of the motor tracts. 
Probably in this way must be explained the hemiparesis on the same side 
as the lesion which has occasionally been noted in cerebellar abscess. In 
the cases which have come within the personal knowledge of the writer 
moderate hemiparesis has been not uncommon. Genuine hemiplegia, on 
the other hand— i.e., actual paralysis—has not been present. 

Focal Symptoms. —It is necessary to state in advance of any discussion 
of the focal symptoms that in many cases they are absolutely wanting. 
In such a case the diagnosis may be exceedingly difficult. On the other 
hand, when focal symptoms are present, there is no intracranial lesion of 
which the clinical picture is more definitely characteristic. Among the 
symptoms entering into this symptom-complex are (1) nystagmus, (2) 
subjective vertigo, (3) incoordination ataxia on the side corresponding to 
the lesion, (4) diadokokinesis (Babinski), (5) loss or impairment of the 
arthrodial sense, or sense of position, (6) disturbance of static equilibrium. 
These phenomena call for brief comment. 

The nystagmus of cerebellar abscess is of distinctly vestibular type,— 
i.e., it is composed of a quick movement in one direction and a slow move¬ 
ment in the other. It is usually rotary in character. Superficially, there¬ 
fore, its resemblance to the nystagmus of labyrinthine disease is complete. 
Its direction, however, is not regularly either toward or away from the 
side of the lesion. Very frequently it is a changing nystagmus, the direc¬ 
tion of the quick component being first to one side and then to the other in 
accordance with the direction in which the eyes are voluntarily turned. 


84 Macewen: Pyogenic Diseases of Brain, etc., p. 195. 





CEREBELLAR ABSCESS: SYMPTOMS 


377 


Usually, however, the nystagmus toward the side of the lesion is stronger 
than the opposite nystagmus induced b} 7 rotating the eyes in the opposite 
direction. It is a progressive or increasing nystagmus, which usually 
shows no tendency to gradual subsidence, but tends rather to become more 
pronounced with the progress of the lesion (Neumann). While, therefore, 
the eve movements are identical in character with those seen in acute 
suppurative labyrinthitis, there are usually certain features which definitely 
differentiate the nystagmus of cerebellar disease from that induced by an 
irritative lesion of the vestibular apparatus. 

Subjective vertigo is a more or less prominent symptom in most cases of 
cerebellar abscess. When nystagmus appears, there is probably at first 
a typical rotary vertigo, presumably induced by the nystagmus. Accord¬ 
ing to Neumann, this subjective rotary vertigo tends to subside as the 
individual becomes inured to a nystagmus which is a stationary or increas¬ 
ing phenomenon of the disease. Even after this rotary nystagmic vertigo 
has disappeared, however, there usually remains a subjective disturbance 
of equilibrium which is quite independent of the nystagmus. It is also a 
fact that certain patients, who exhibit no nystagmus, yet suffer from 
more or less constant dizziness, or vertigo. I believe that this is an 
important symptom in certain cases in which the more characteristic 
focal signs are absent. That is to say, in a case of intracranial lesion with¬ 
out definite localizing symptoms, persistent vertigo would point, other 
conditions being equal, to the cerebellum as the probable site of the lesion. 

Unilateral incoordination ataxia is usually present in cases in which 
any clear focal signs are demonstrable. It is shown by a lack of precision 
in certain movements of the hand and arm of the side corresponding to 
the brain lesion. It is best elicited by the common experiment of requiring 
the patient with eyes closed to touch the tip of the nose quickly first with 
the tip of the right forefinger and then with the left. It will be found that, 
while he can execute this movement with ease and precision with the 
finger corresponding to the sound side of the brain, the forefinger corre¬ 
sponding to the side of the lesion may miss the nose by some inches and is 
brought into contact with it only after a series of to-and-fro oscillations in 

its immediate vicinity. # . . 

Diadokokinesis (Babinski ).—Regularly with incoordination ataxia will 

be associated the condition known as diadokokinesis. If we direct the 
patient to practise any common movement of the two hands, fingers, or 
wrists simultaneously,— e.g. } the finger movements as in piano practice,— 
it will be found that the one hand executes these movements quickly and 
with normal ease while the fingers of the hand corresponding to the cere¬ 
bellar lesion execute the same movements in normal enough rotation, but 
slowly and with apparent labor. If we vary this experiment Dy asking him 
to rotate both wrists as rapidly as possible back and forth, the one wrist 
will be rotated rapidly while the other—corresponding to the side of 
the lesion—follows with similar rotations performed very slowly. In a 
case of right-sided cerebellar abscess coming under the writer’s care, the 


378 


INTRACRANIAL LESIONS OF OTITIC ORIGIN 


left wrist executed just four rotations while the right rotated once,^ 
a ratio which for the average normal individual would be rather a 
difficult feat. 

Loss or Impairment of Arthrodial Sense, or Sense of Position. —This may 
be tested by blindfolding the patient, passively moving the arm or leg cor¬ 
responding to the lesion in different directions, and leaving it in some 
unusual position. He is then directed to duplicate its position with the 
corresponding opposite limb. Inability to do so shows loss of position or 
posture sense on the side corresponding to the lesion. It is a corroborative 
sign which, I believe, is often absent when other definite focal symptoms 
are present. 

Disturbance of Equilibrium; Cerebellar Ataxia. —I have seen cases of 
cerebellar abscess in which the patient has been able to stand and walk 
steadily and without noticeable difficulty in maintaining his equilibrium. 
In other cases—and always when other focal symptoms are present—dis¬ 
turbance of static and dynamic equilibrium is a more or less prominent 
symptom. 

In speaking of the ataxia of cerebellar abscess, Neumann states that 
“it stands in exact physiological relationship, demonstrable every mo¬ 
ment, to the direction of the nystagmus and the position of the head in 
regard to the body. If, for example, rotary nystagmus toward the left 
side is present, the patient leans toward the right on standing erect/’ 
etc . 35 This conception of cerebellar ataxia is one which, in the opinion 
of the writer, will not be borne out by a careful study of any large series 
of cases. 

With the first appearance of cerebellar nystagmus, subjective rotary 
vertigo resulting directly therefrom is probably always present, and this 
rotary vertigo may to some extent influence the patient’s tendency to fall 
in a given direction. But it is admittedly a characteristic feature of cere¬ 
bellar nystagmus that the related rotary vertigo tends to subside and 
finally to disappear. With disappearance of the nystagmic vertigo, the 
persisting ataxia can hardly be ascribed to the nystagmus, and as a matter 
of fact it may show no relation to the eye movements. I can illustrate this 
point by a case of cerebellar abscess of which I had the opportunity to 
make a very careful study . 36 This patient exhibited a nystagmus increasing 
with the progress of the lesion, and changing its direction in accordance 
with the direction in which the eyes were voluntarily turned, but very much 
more pronounced in the direction of the side of the lesion. So far as I 
could observe, and from the patient’s statements, the nystagmus had little 
or no influence upon her subjective vertigo. When the patient attempted 
to stand she fell, or without support would have fallen, to the right,— i.e., 
toward the side of the lesion. Throughout her illness her tendency to fall 
to the right was constant, which, it will be noted, was exactly opposite to 


35 Neumann: Cerebellar Abscess, Lake’s translation, p. 23. 
38 Kerrison: Annals of Otol., March, 1911. 





CEREBELLAR ABSCESS: DIFFERENTIAL DIAGNOSIS 379 


what should have been her direction of falling in relation to the nystagmus 
present. I believe that this is an important feature of the characteristic 
ataxia of cerebellar abscess,—viz., that, when disturbance of equilibrium is 
a prominent and constant symptom, the direction in which the patient falls, or 
tends to fall, is conctant and is for the most part independent of the nystagmus 
present. Nor should this surprise one, for with incoordination ataxia, 
disturbed arthrodial sense, and in some cases hemiparesis, all confined to 
one side of the body, it seems not illogical to expect that these condi¬ 
tions should be not without influence in determining the direction in 
which the patient may fall. Logically, an ataxia which is not dependent 
upon an existing nystagmus, or in a case in which spontaneous nystagmus 
is not present, will not be influenced by changes in the position of the 
patient’s head. 

Naturally all symptoms may be modified or masked as the terminal 
stage is approached, when the patient’s muscular reactions may be ob¬ 
scured to a point where, if placed upon his feet, he will fall in any direction 
according to the influence of gravity as determined by the chance position 
of his body. 

Other symptoms of cerebellar abscess which, though inconstant, are 
characteristic and add when present to the completeness of the clinical 
picture, are frequent involuntary yawning, and slow, thick articulation. 

An important group of focal symptoms which logically belongs here is 
that which includes the various disturbances of normal pointing accuracy, 
sometimes properly spoken of as “past pointing. Their appreciation, 
however, is so clearly dependent upon a knowledge of Professor Barany’s 
theory of cerebellar localization, that it seems better to devote a separate 

chapter to their consideration (Chapter XIV). 

The Terminal Stage. —In its terminal stage a fatal case of cerebellar 
abscess may present much the same clinical phenomena as those already 
described in connection with temporosphenoidal abscess. The most 
characteristic difference is found in the respiratory changes, which are not 
very common in cerebral abscess but are particularly characteristic ot 
cerebellar lesions. As death approaches the breathing may become slow, 
sighing, or even Cheyne-Stokes in character, or it may be simply ster¬ 
torous.' The end may come only with the final exhaustion of the patient’s 
last vestige of vitality and resistance power, or may be hastened by rupture 
of the abscess into the subarachnoid space. In either case the immediate 

cause of death is usually respiratory paralysis. 

Differential Diagnosis. —The two lesions for which otitic cerebellar 
abscess may be mistaken are temporosphenoidal abscess and acute diffuse 
suppurative labyrinthitis. When focal symptoms are absent it may very 
closely resemble a temporal-lobe abscess. With the appearance of focal 
symptoms the resemblance to cerebral abscess recedes, and the necessity 
for excluding suppurative labyrinthitis arises. 

Differential Diagnosis between Temporal-lobe and Cerebellar Abscess — 
Since either of these lesions may run its course with almost complete 


380 


INTRACRANIAL LESIONS OF OTITIC ORIGIN 


absence of localizing symptoms, it may be necessary to weigh carefully 
even minor points which may throw light upon the site of the lesion. 

Headache, for example, is common to both lesions. The headache of 
cerebellar abscess, however, is on the average more severe, less subject 
to periods of amelioration, and is more frequently confined to the occipital 
region on the side of the lesion. Vomiting characterizes the onset of both 
lesions. After the initial stage, vomiting is exceedingly rare as a result of 
temporal-lobe abscess, whereas it not infrequently recurs at indefinite 
intervals throughout the course of a cerebellar abscess. Mental dulness or 
obscuration, as shown by delayed or slow cerebration, failure of the power of 
sustained attention, etc., is a characteristic and in some cases a fairly early 
symptom of temporosphenoidal abscess. It is comparatively uncommon in 
cerebellar abscess, and rarely appears except as a late symptom and in 
company with other evidences of marked increase in general intracranial 
pressure. Eye-ground changes —papillitis, choked disk, or optic neuritis— 
are very much more common in cerebellar than in cerebral abscess, a fact 
which in certain cases may have some diagnostic significance. Muscular 
paresis, when present in temporosphenoidal abscess, is always contralateral. 
Hemiparesis on the same side of the body has frequently been noted in 
cerebellar abscess. Vertigo in temporal-lobe abscess is usually an incon¬ 
stant and rather indefinite symptom, depending upon increase in general 
intracranial pressure. Noticeable disturbance of static equilibrium is not 
usually present in the early stages of the lesion. On the other hand, the 
vertigo and ataxia of cerebellar abscess may appear as prominent and 
fairly early symptoms. That is to say, the subjective disturbance is per¬ 
sistent, and the ataxia is usually characterized by a constant tendency to 
fall in a given direction. 

When focal symptoms are present, the diagnosis becomes a compara¬ 
tively easy matter. Thus, sensory aphasia —especially if occurring early 
in the course of a suspected intracranial lesion—points fairly definitely to a 
lesion of the left cerebral hemisphere, or, in the case of a left-handed indi¬ 
vidual, to the right brain. Aphasia does not occur in cerebellar abscess 
except as a late symptom and only in cases in which other signs of very 
marked general increase in intracranial pressure are present. Naturally, 
when focal symptoms of cerebellar abscess are well marked,— -e.g., cerebel- 
lai nystagmus and ataxia, incoordination ataxia, and disturbed arthrodial 
sense on the side corresponding to the lesion,—the case no longer presents 
difficulties of diagnosis. 

The differential diagnosis between cerebellar abscess and diffuse suppura¬ 
tive labyrinthitis usually presents little or no difficulty to the careful student 
of labyrinthine and intracranial diseases. When focal symptoms of cere¬ 
bellar abscess are absent, the clinical phenomena of this lesion in no way 
resemble those of suppurative labyrinthitis. Again, when the acute stage 
of suppurative labyrinthitis is passed, all clinical resemblance to cerebellar 
abscess ceases. When, however, focal symptoms of cerebellar abscess are 
present, this lesion and the acute stage of suppurative labyrinthitis may 


CEREBELLAR ABSCESS: DIFFERENTIAL DIAGNOSIS 381 


present certain points in common,— e.g., nystagmus, vertigo, static ataxia, 
vomiting, etc.,—which might lead to serious error. The chief differential 
points are briefly stated below. 


Diffuse Suppurative Labyrinthitis 
(Acute Stage). 

Rotary nystagmus toward sound ear; 
is always increased when eyes are volun¬ 
tarily turned toward sound ear,— i.e., in 
the direction of quick eye movement, being 
diminished or disappearing wholly when 
they are turned in the direction of the slow 
eye movement. 

The nystagmus tends regularly toward 
gradual subsidence, and usually disappears 
wholly in from 10 days to 2 or 3 weeks. 

Subjective rotary vertigo, always in the 
plane of the nystagmus, is increased when 
the eyes are turned in the direction of the 
quick eye movement; shows progressive 
diminution, and ceases wholly when the 
spontaneous nystagmus has completely 
disappeared. 

Ataxia: there is a tendency to fall in the 
plane of the nystagmus and in the direction 
opposite to the quick nystagmic movement. 
This disturbance of equilibrium regularly 
subsides, and ceases wholly when the 
nystagmus has disappeared. 

Impairment of the touch-direction- 
sense; effort to point with either hand, eyes 
being closed, resulting in deviation in a 
direction opposite to that of the quick 
nystagmic movement. 30 * 


Caloric reaction absent. 

Hearing absolutely lost in diseased ear. 

Incoordination ataxia and diadokokine- 
sis absent. 

Arthrodial sense/or sense of joint posi¬ 
tion, not usually impaired. 

Temperature, elevated at onset, shows 
in uncomplicated cases progressive and 
fairly rapid recession. Rarely subnormal. 

Pulse-rate may be normal, or varies in 
normal ratio with temperature changes. 


Cerebellar Abscess. 

Changing rotary nystagmus,— i.e., di¬ 
rection of quick eye movement may vary 
at different times; frequently changes in 
accordance with the direction in which the 
eyes are voluntarily turned. Usually, 
however, the most pronounced eye move¬ 
ments observed are those toward the side 
of the lesion. 

There is no tendency toward subsidence, 
the nystagmus usually becoming more 
marked with the progress of the lesion 
(Neumann). 

Vertigo, at first influenced by the nys¬ 
tagmus, later ceases to be influenced 
thereby. Subjective vertigo is often pres¬ 
ent and persistent, even in cases in which 
nystagmus is not present. 

The ataxia, as a rule, shows no tendency 
to subside. Direction of falling is usually 
constant, and has no necessary relation to 
character or direction of nystagmus pres¬ 
ent. 

When other focal symptoms are absent, 
touch-direction-sense, shown by accuracy 
in pointing with eyes closed, may be un¬ 
impaired. With focal symptoms, loss of 
accuracy in pointing— i.e., deviation of 
hand to one side or the other—is usually 
present, but only in the hand or finger of 
same side as the cerebellar lesion. 

Caloric reaction usually normal. 

Hearing normal, or at least not influ¬ 
enced by cerebellar disease. 

Incoordination ataxia and diadokokine- 
sis may be prominent symptoms. 

Arthrodial sense may be lost, or mark¬ 
edly impaired. 

Temperature, elevated at onset, usually 
recedes, and may then follow a fairly 
normal line, or may show moderate move¬ 
ment between points a little above and 
slightly below normal. 

Pulse-rate is not infrequently abnorm¬ 
ally slow. Bradycardia may coexist with 
elevation of temperature. 


3tt a For theorv and significance of pointing, see next Chapter. 





382 INTRACRANIAL LESIONS OF OTITIC ORIGIN 

When the latent stage of diffuse suppurative labyrinthitis is reached 
the disease no longer bears any resemblance to cerebellar abscess. The 
differential diagnosis is then definitely established by the complete deaf¬ 
ness and absence of caloric irritability in the diseased ear in suppuiative 
labyrinthitis, hearing and vestibular irritability i.e., in response to heat 
and cold—being usually uninfluenced by cerebellar abscess. 


OTITIC MENINGITIS. 

Otitic meningitis is an elastic term which may very properly include a 
variety of conditions, from the circumscribed pachymeningitis, which 
commonly yields very promptly to rational treatment, to the diffuse, or 
generalized, purulent leptomeningitis, which ends in death. 

Circumscribed Pachymeningitis. —This condition may be dealt with 
briefly. Every aural surgeon of considerable experience has during opera¬ 
tion upon the mastoid met with occasional cases in which circumscribed 
areas of dura have been found thickened, congested, or even covered with 
granulations. The condition is not infrequently met with as part of the 
pathology of an extradural abscess, or it sometimes results from an ero¬ 
sion of the inner plate of the skull even when no distinct pus collection is 
found. Such areas of pachymeningitis may involve the dura over the 
tegmen antri (temporal lobe), the dural covering of the sigmoid sinus, or 
less frequently the dura covering the cerebellum. Frequently the con¬ 
dition is not suspected prior to operation. In the occasional cases in 
which severe pain leads to a tentative diagnosis of intracranial disease be¬ 
fore operation, the pain is usually due to tension upon the dura by a con¬ 
siderable collection of pus rather than to the inflammatory process itself. 
The great majority of cases undergo prompt resolution as soon as all dis¬ 
eased bone is removed and the inflamed dural surface is freely uncovered. 
The subsequent treatment is simply the observance of surgical cleanli¬ 
ness, the wound being lightly packed at each change of dressing with 
sterile gauze until the involved dural surface is covered by a layer of uni¬ 
formly healthy granulations. 

So frequently is circumscribed pachymeningitis met with in cases in 
which no meningeal symptoms have been present, and so prompt is the 
usual response to treatment, that one might be led into the error of belit¬ 
tling the gravity of the lesion. It is a simple lesion only under prompt 
rational treatment. Without surgical intervention it is undoubtedly the 
precursor in many cases of the more serious lesions which jeopardize the 
patient’s life. 

Leptomeningitis resulting from suppurative middle-ear or mastoid 
disease, and producing symptoms sufficiently characteristic to be recog¬ 
nized as meningeal, was once regarded as an absolutely hopeless condition. 
During the past ten or fifteen years, however, the record of authenticated 
recoveries has reached a sufficient number to necessitate a modification of 
this view as to the hopelessness of the prognosis in all cases. In order to 
explain the varying response to treatment in cases often closely related 


DIFFUSE PURULENT LEPTOMENINGITIS 


383 


clinically, it is necessary to bear in mind certain variations in the character 
or extent of the morbid changes present, in accordance with which we may 
recognize the existence of different types or forms of the disease. 

The three most important forms of otitic meningitis may be described 
under the following names: (1) Diffuse, or generalized, purulent lepto¬ 
meningitis; (2) circumscribed purulent leptomeningitis; and (3) serous 
meningitis. While it is admittedly not always possible to determine defi¬ 
nitely from its clinical aspects to what class a given case belongs, there are 
some cases in which this may be determined with reasonable certainty. 
Furthermore, the recognition of the existence of the three forms supplies a 
useful working hypothesis, and enables us to adopt rational methods of 
treatment resulting in a certain percentage of recoveries in cases which 
would otherwise terminate fatally. 

Diffuse Purulent Leptomeningitis. —By diffuse purulent leptomen¬ 
ingitis we mean a suppurative inflammation of the meninges which has 
reached the subdural and subarachnoidal spaces, involving the arachnoid 
and pia mater, and which has spread widely— i.e., with no tendency to 
limiting peripheral adhesions—within the meshes of the arachnoid. 

The pia mater is very richly supplied with nerves and blood-vessels, 
its arteries separating into very numerous branches which pass directly 
into the brain cortex. A suppurative process involving the pia mater is 
thus carried directly into the outer layer of brain substance. Severe diffuse 
purulent leptomeningitis is, therefore, of necessity accompanied by a 
cortical encephalitis. 

Paths of Infection. —The spread of infection from a suppurative 
focus in the middle ear or mastoid may occur by any of the following routes: 
(1) By direct infection through contact of necrotic bone with the dura, or 
through erosion of the inner plate at some point,— e.g., of the tegmen 
tvmpani or the bony plate separating the mastoid cavity from the cere¬ 
bellum. In such a case the meningeal lesion probably always begins as a 
circumscribed pachymeningitis. (2) Through an infected labyrinth, pus 
reaching the meninges (a) by way of the nerve channels opening into the 
internal auditory meatus; (b) by the aquseductus vestibuli, causing first 
an empyema of the saccus endolymphaticus; or (c) by way of the aquse¬ 
ductus cochleie, which, it will be remembered, communicates directly 
with the subarachnoidal space. (3) A third pathway of infection is through 
an intermediate suppurative lesion of the brain. Every experienced sur¬ 
geon will agree that a very considerable proportion of all fatal cases of brain 
abscess are toward the end complicated by purulent meningitis. 

Symptoms. —The symptoms of otitic meningitis do not differ mate¬ 
rially from those induced by meningeal inflammations arising from other 
causes. They may, therefore, be dealt with briefly. The onset is usually 
announced by a chill, or rigor, a sharp rise of temperature, and in many 
cases by vomiting, with or without nausea. Headache, always an early 
symptom,.is usually severe and may persist throughout the course of the 
disease. The pulse is usually accelerated, in adults reaching 120 to 140, 


384 


INTRACRANIAL LESIONS OF OTITIC ORIGIN 


while in children it may be even more rapid. The face is often noticeably 
flushed. The patient is usually exceedingly restless, and frequently ex¬ 
hibits an irritability of temper which may be in striking contrast to his 
normal mental state. These symptoms, then, viz., recurrent vomiting, 
severe headache, high fever, rapid pulse, and restlessness, commonly 
characterize not only the onset, but also the first two or three days of 
the attack. The clinical picture even to the superficial observer is one of 
severe illness, and in a case of tympanic or mastoid disease clearly indi¬ 
cates a serious change for the worse. 

Usually by the second or third day we have the following additional 
symptoms: There is noticeable rigidity of the muscles of the back of the 
neck. This soon increases to the point where, if one tries to flex the head 
forward so that the chin will rest upon the sternum, this is resisted, and we 
may to some extent lift the shoulders before the neck muscles will yield. 
Kernig’s symptom is often, though not always, present,— i.e., if the knee 
is bent and the thigh flexed toward the abdomen, passive straightening of 
the leg is rigidly resisted. Photophobia becomes sooner or later a notice¬ 
able symptom. The mental condition, from one of extreme “restlessness” 
or “irritability,” soon lapses into delirium. Delirium, at least during the 
night, is usually a fairly early symptom in diffuse meningitis. From this 
stage, the course of the disease is usually an exceedingly rapid one and 
provides one of the most distressing and discouraging pictures of fast 
ebbing of the life current that the physician is called upon to witness. The 
patient tosses distressfully about the bed, happily without knowledge of his 
condition and often, it is to be hoped, without conscious suffering,—the 
extreme restlessness subsiding only as he gradually sinks into coma, the 
immediate precursor of death. 

Pupillary changes are very common, the most frequent being contrac¬ 
tion of the pupil corresponding to the side of the lesion. Occasionally there 
is strabismus, usually inward. The pupillary changes, while in some 
instances affecting both eyes to some extent, in the majority of cases are 
unilateral or more marked in the eye on the side of the lesions. 

Changes in the eye-grounds— e.g., choked disk, papillitis, optic neuritis 
—are very often present in diffuse leptomeningitis. 

The above group of symptoms, while fairly typical of the average 
course of the disease, is naturally subject to many clinical variations. It 
must be remembered that the onset, as we recognize it, may not represent 
the incipiency of the lesion, but simply its first clinical manifestation. 
Rigidity of the neck, photophobia, and even delirium may, therefore, in 
some degree be noticeable almost from the start. The pulse, which is 
usually very rapid, is in exceptional cases abnormally slow,— e.g., 64 or 
60 beats per minute or less,—this phenomenon being presumably due to a 
coincident cortical encephalitis with possible disturbance of some centre 
inhibiting cardiac activity. 

One of the most characteristic features of the clinical picture of diffuse 
purulent meningitis is the sudden and striking change which occurs in the 


CIRCUMSCRIBED LEPTOMENINGITIS 


385 


patient’s appearance at a certain stage of the disease. To-day he looks 
out upon the world through intelligent eyes, showing anxiety about 
his condition and perhaps a realization of its gravity. To-morrow he 
is delirious and has stamped upon his face the unmistakable sign of 
impending death. 

Blood Count .—A characteristic feature of purulent meningitis is a 
high and increasing leucocytosis with a high percentage of polymorpho¬ 
nuclear cells. 

Lumbar Puncture .—In the first stages of a meningeal attack, lumbar 
puncture may furnish the only reliable data as to the nature and gravity of 
the lesion. That is to say, the presence of pus and bacteria in the spinal 
fluid may point definitely to purulent meningitis at a stage when the clin¬ 
ical picture is yet incomplete. 

Prognosis. —When a suppurative leptomeningitis has become diffuse,— 
i.e., has spread widely in the meshes of the arachnoid,—death is inevitable. 

Circumscribed Leptomeningitis. —This term is used to describe a 
suppurative inflammation involving the arachnoid and pia mater over a 
distinctly limited area, lateral extension being prevented by marginal ad¬ 
hesions binding the arachnoid and pia together and to the outer dural 
layer; or it may be that marginal extension is in some cases prevented by 
the combination of a mild local infection with high powers of local resist¬ 
ance. The marginal limitation of the lesion, while preventing the devel¬ 
opment of widespread, or diffuse, leptomeningitis, does not necessarily 
insure that some of the germs responsible for the infection shall not find 
their way into the fluid of the spinal canal. Lumbar puncture may, there¬ 
fore, yield fluid containing pus and bacteria, and the presence of pus and 
bacteria in the cerebrospinal fluid may constitute no proof of the existence of 
what may properly be called diffuse purulent leptomeningitis. 

Unfortunately, the symptoms of circumscribed leptomeningitis may 
follow practically the same course and sequence as those described as 
characteristic of "diffuse leptomeningitis. Assuming that the lesion remains 
circumscribed, we might expect the progress of the disease to be less rapid, 
and this is undoubtedly a differential clinical point in certain cases. Un¬ 
fortunately, even were we able to determine positively in a given case the 
circumscribed character of the disease, there would be no way of determin¬ 
ing that adhesions might not at any moment be broken down and the dis¬ 
ease thus quickly converted into a widely spreading, and therefore rapidly 
fatal, form of diffuse leptomeningitis. 

There can be no doubt that many cases of circumscribed leptomeningitis 
of otitic origin, which would otherwise have ended fatally, have been cured 
by timely operative intervention. This proposition is no longer an hypothe¬ 
sis, many authenticated recoveries recorded during the past ten or fifteen 
years supplying a basis of actual knowledge. Jansen, 37 as far back as 1895, 
recorded a recovery in a case in which the lesion was clearly proved to be 


37 Jansen: Berlin, klin. Woch., 1895, No. 35, pp. 7G3 765. 


25 





386 


INTRACRANIAL LESIONS OF OTITIC ORIGIN 


circumscribed leptomeningitis. This patient, having suffered for years 
from chronic suppurative otitis media of the left ear, suddenly had a chill, 
high fever, and severe headache. Coincidently he developed symptoms of 
sensory aphasia which naturally led to a tentative diagnosis of abscess of 
the left temporal lobe. Following quickly upon the symptoms mentioned, 
the patient became delirious. An exploratory operation for temporo- 
sphenoidal abscess was then undertaken. No abscess was found in the 
brain, but the dura and pia were discolored, adherent, and a drop of pus 
escaped from beneath the dura when the membranes were incised. Re¬ 
covery proved the condition to have been one of circumscribed lepto¬ 
meningitis. 

Lucae 38 in 1899 reported a case in which the diagnosis of otitic menin¬ 
gitis was based upon the symptoms. At the operation the exposed dura 
presented an area of greenish discoloration, from the meshes of which, 
when incised, pus exuded. The patient made a slow but perfect recovery. 

Gradenigo 39 has reported two cases presenting typical symptoms of 
leptomeningitis, in which the fluid from the spinal canal contained sta¬ 
phylococci, which recovered after operation. 

Similar cases have been recorded in this country by Arnold Knapp, 49 
McKernon, 41 Kopetsky-Held, 42 and others. These cases, cited at random 
from the literature, are sufficient to establish this important fact,—viz., 
that there are certain cases of purulent leptomeningitis of otitic origin 
which are curable by surgical means. This naturally introduces the 
question as to what type of purulent leptomeningitis is curable and in 
what class is the prognosis hopeless. Some surgeons—among whom are 
Lemoyes and Gradenigo—have regarded the cases recovering after opera¬ 
tion as cases of diffuse leptomeningitis, and have naturally, therefore, held 
a more optimistic view as to the prognosis in the diffuse form of the disease. 
On the other hand, Heine cites Hinesberg, Bertelsmann, Buschmann, and 
Grossmann (most of whom have operated successfully in cases of otitic 
meningitis) as sharing with him the opinion that all these cases of recovery 
have belonged to the circumscribed form of purulent meningitis, and that 
diffuse suppurative leptomeningitis is a hopelessly fatal disease which the 
surgeon is powerless to relieve. To the writer this view seems to be the 
only one tenable. Several cases of recovery from otitic meningitis have 
come within his personal knowledge, but none in which a positive diagno¬ 
sis of diffuse suppurative leptomeningitis could be made. We must remem¬ 
ber that in the diffuse form of the lesion the infection travels marginally 
through the communicating spaces, or meshes, of the arachnoid (Hins- 
berg). When we recall the postmortem findings as we have all seen them 
in some case of rapidly fatal diffuse meningitis,—the arachnoid adherent 


38 Lucae: Berlin, klin. Woch., 1899, No. 23, pp. 497-499. 

39 Gradenigo: Arch, fur Ohrenheil., Bd. 47, p. 155. 

40 Knapp, A.: Arch, of Otology, vol. xxxv, No. 1. 

41 McKernon: Arch, of Otology, vol. xxxvii, No. 3 and 4, 1908, pp. 183-189. 

42 Kopetsky-Held: Arch, of Otology, vol. xxxv, No. 6. 



SEROUS MENINGITIS 


387 


over a wide area both to the dura and the pia mater, and its meshes every 
where infiltrated with thick pus,—the hopelessness of surgical treatment 
seems clear. 

Serous Meningitis; Serous Meningo=encephaIitis (Korner).—Still 
another form of meningeal lesion of otitic origin is that known as serous 
meningitis. It may be secondary to a circumscribed pachymeningitis 
such as frequently occurs with extradural abscess. Quite frequently, 
however, no such intermediate lesion is in evidence. Serous meningitis 
is present in those cases of meningeal inflammation in which the arachnoid 
and pia mater, though congested and oedematous, have escaped actual 
infection. This secondary oedema may involve the adjacent brain surface 
(serous encephalitis), and may cause very considerable increase in intra¬ 
cranial pressure. The symptoms may follow very closely those of diffuse 
purulent leptomeningitis. A differential point between serous and purulent 
meningitis is the fact that pus and bacteria are not found in the cerebro¬ 
spinal fluid in purely serous meningitis. On the other hand, bacteria may 
also be absent from the spinal fluid in cases of purulent meningitis. Lum¬ 
bar puncture, while supplying very important data, does not, therefore, 
always enable us to arrive at a positive diagnosis. In a case coming under 
the writer’s care, the clinical picture was quite typical of purulent menin¬ 
gitis, and this diagnosis was made by competent surgeons in consultation. 
That it was really a case of serous meningitis was determined only after 
the patient’s recovery was assured. Indeed, one of the most important 
points in the diagnosis of serous meningitis is the recovery of the patient. 

The symptoms vary somewhat in accordance with the depth to which 
the subdural tissues are involved. Thus, when the congestion and oedema 
involve only the arachnoid and pia mater, the symptoms are meningeal 
in character, this constituting serous meningitis in its most typical form. 
In such a case the clinical phenomena may be practically the same in kind 
as those usually characterizing purulent leptomeningitis. If, however, 
the oedema extends well into the subjacent cerebral cortex, a train of 
symptoms more characteristic of cerebral disease— e.g., somnolence, re¬ 
tarded cerebration, or possibly aphasic phenomena—may preponderate. 
To such a lesion the term serous encephalitis has been applied. 

Perhaps a brief outline of a few typical cases will serve better to convey 
a correct idea of the lesion than any amount of formal description. 

Case I.—In June, 1904, the writer was called to see a girl of five years, 
who was suffering from acute suppurative mastoiditis of the right side. 
The lesion had reached a stage (postauricular abscess) requiring immediate 
operation. Removal of the cortex revealed pus and granulations in the 
antrum and many of the mastoid cells. Three days later, severe headache 
was complained of, the temperature rose to 104° F., the neck became 
somewhat rigid, and the child became delirious. On the following day 
there was internal strabismus. Dr. A. B. Duel in consultation concurred 
in the diagnosis of otitic meningitis. An immediate operation was per¬ 
formed, which consisted merely of careful exposure of the dura covering 



388 


INTRACRANIAL LESIONS OF OTITIC ORIGIN 


the temporal lobe by removal of the tegmen tympani et antri and con¬ 
tiguous portions of the squama. The dura showed no structural changes 
macroscopically, and it was decided to await further developments before 
incising it. Following this operation, the meningeal symptoms began 
to subside, and the patient made a perfect recovery. The S3'mptoms 
in this case can be explained only as having been caused by a serous 
meningitis. 

Case II was that of a young woman, twenty-three years of age, who 
came under my care as a ward patient in the Manhattan Eye, Ear, and 
Throat Hospital in 1907. A radical operation for chronic suppuration of 
the right ear had been performed one year previously in a neighboring 
city. At the time of her admission to the Manhattan Hospital, her con¬ 
dition was about as follows: There was a slight discharge from the right 
ear. There were no focal symptoms pointing to any particular intracranial 
lesion. Mental condition decidedly dull, cerebration somewhat obscured, 
but she answered all questions intelligently. She was disinclined to any 
muscular exertion, and when required to stand or walk was noticeably 
unsteady. The patient’s lack of interest in her surroundings and in her 
own condition extended to the matter of food: she was without appetite 
and it was difficult to induce her to take sufficient nourishment. Loss of 
flesh and strength was therefore rapid. Temperature ranged between 
100° and 101° F. 

The above symptoms, though indefinite, seemed to me to suggest 
abscess of the right temporal lobe rather than any other lesion, and I 
determined upon an exploratory operation. The dura covering the tempo- 
rosphenoidal lobe was freely exposed by the removal of a considerable 
portion of the squama. No macroscopic changes in the dura were noted. 
A narrow-bladed knife was inserted into the temporal lobe in three 
different directions, but no abscess was found, and the operation was 
ended here. To the surprise of the writer, the patient from the time of 
this operation showed progressive improvement, and was discharged, 
cured, within a month. The clinical phenomena in this case can be 
explained upon no other hypothesis than that they were due to a serous 
encephalitis. 

Case III 43 has been reported in full elsewhere, and will be given here 
only in brief outline. Mr. C., thirty-four years of age, had suffered from 
early childhood with chronic suppurative otitis media of the left side. On 
June 4, 1907, he had experienced severe pain in the left ear. On the fol¬ 
lowing morning, when I first saw him, the temperature had reached 103° 
F., pulse 120. He had vomited at frequent intervals. Mental condition 
dull, but he answered correctly all direct questions. By the afternoon of 
the same day, he had become delirious, and did not recognize even mem¬ 
bers of his own family. There was some rigidity of the muscles of the neck. 
The pupils were contracted to pin-points. Two other, physicians, called 


43 Iverrison: Arch, of Otology, vol. xxxvii, No. 2, 1908. 



MENINGISMUS 


389 


in consultation, confirmed the diagnosis of otitic meningitis and advised 
immediate operation, which was performed as soon as the patient could be 
prepared. 

Operation .—A radical operation was quickly performed, revealing a 
sclerotic bone and an antrum filled with thick, offensive pus. The roof 
of the antrum and portions of the squama were then removed, exposing 
an area of dura covering the temporosphenoidal lobe .measuring from 
before backward about three inches. No pus was found between dura and 
bone. Increase in cerebral pressure shown by bulging of exposed dura. 
Dura somewhat engorged,— i.e., showed small areas of capillary injection. 

The dura was now opened by three parallel, vertical incisions about 
one inch apart. Considerable oozing of cerebral fluid followed. Through 
each of these incisions a narrow knife was successively introduced into 
the brain substance, that through the posterior incision reaching the 
lateral ventricle and giving exit to a considerable flow of cerebral fluid. 
This completed the operation. Loose sterile gauze was placed in contact 
with the incised dura, this being covered by a large sterile dressing. 

On the following morning, the patient’s temperature was 98.6° F., 
pulse 78. He complained of severe headache, but his mental condition 
was quite clear. He retained no memory of the happenings of the preced¬ 
ing day, which has remained a blank in his experience. For some weeks 
following the operation, there was a rather copious loss of cerebral fluid 
which ceased only when the dural openings finally closed. The patient 
made a complete recovery. In this case we have a perfect example of a 
severe type of serous meningitis which would undoubtedly have ended 
fatally but for the prompt and rather drastic surgical treatment. 

Meningismus.—Before leaving the discussion of meningeal disorders 
which may have an otitic origin, passing mention should be made of a 
condition in which, without actual invasion by infective organisms 
and without grave pathologic change, the meninges are subjected to cer¬ 
tain transitory irritative influences of sufficient violence to induce symp¬ 
toms almost or practically identical with those characteristic of a severe 
meningeal inflammation. To this condition, the pathology of which is not 
clearly known, the name meningismus is applied. It may be induced, 
particularly in young children, by a purulent otitis media or mastoiditis, 

but is probably much oftener due to other causes. 

Differential Diagnosis. —Having described briefly the three main 
types of otitic meningitis, one is forced to admit that it is rarely possible at the 
beginning of a meningeal attack to determine to what group it will prove 
ultimately to belong. It is probable that it will never be possible to make 
an early positive differential diagnosis between a circumscribed and a 
diffuse purulent leptomeningitis. Yet the importance of endeavoring to 
arrive at a correct diagnosis as early as possible will hardly be questioned. 
Everyone knows the inherent danger in the practice of any special 
branch of medicine,— i.e., of viewing all diseases from the cramped and 
narrow confines of that specialty. While by no means an invariably 


390 


INTRACRANIAL LESIONS OF OTITIC ORIGIN 


reliable index, it is beyond question that the character of the spinal fluid 
will supply in many cases of meningeal disorder the most definite diagnostic 
data at our disposal. To give such data their broadest value and use¬ 
fulness, it is clear that the physician should have in mind not only the 
recognized types of otitic meningitis, but should consider as well since 
intercurrent and quite unrelated lesions are always a possibility whatever 
other conditions might give rise either to the clinical symptoms present 
or to changes in the character of the spinal fluid. It may serve a useful 
purpose, therefore, to state briefly (1) the character of the normal cerebro¬ 
spinal fluid; and (2) some of the commoner disorders or lesions in which 
its character may undergo change. 

The Cerebro-spinal Fluid in Health and Disease. —The conditions 
which an examination of the spinal fluid may help to differentiate are (a) epi¬ 
demic cerebro-spinal, or meningococcic, meningitis; (b) purulent meningitis, 
circumscribed or local, i.e., due to infection by other micro-organisms; 
(c) tuberculous meningitis; (d) meningismus; and (e) in times of epidemic, 
and probably always in the larger cities, anterior poliomyelitis. 

A normal fluid is perfectly clear. During lumbar puncture, it flows 
slowly,— i.e., about 10 to 15 drops to the minute. 

In practically all diseased conditions involving the meninges, the spinal 
fluid is increased in amount. 

A perfectly clear spinal fluid under pressure,— i.e., showing considerable 
increase in amount—may mean meningismus, tuberculous meningitis or 
anterior poliomyelitis. It may also indicate syphilis of the spinal cord. As 
occasional exceptions to the above, slight cloudiness of the fluid is seen in 
certain cases of poliomyelitis and tuberculous meningitis. 

Markedly cloudy fluids usually indicate meningitis due to the meningo¬ 
coccus (epidemic cerebro-spinal m.) or to any of the pyogenic micro¬ 
organisms (purulent m.). It is conceivable, however, that an inflammatory 
process in tympanum or mastoid might spread by continuity of tissue to the 
meninges without actual invasion by the pyogenic organism present. Such 
a lesion might give a cloudy fluid (serous meningitis). 

In meningismus the cell count is not usually increased,— i.e., not more 
than one cell to four or five fields is usually found. 

In purulent meningitis, meningococcic meningitis and tuberculous 
meningitis, the cells are increased. The following differences, however, are 
to be noted, viz., (1) the cell increase is as a rule much greater in purulent 
or in epidemic cerebro-spinal meningitis than in tuberculous meningitis; 
and (2) in purulent and in meningococcic meningitis the polymorphonu¬ 
clear cells preponderate by nearly 100 per cent., whereas in tuberculous 
meningitis, the mononuclear cells preponderate in nearly equal ratio 
(95 per cent.). 

There is an increase in the albumen and globulin in the spinal fluid from 
cases of tuberculous, meningococcic and purulent meningitis. There is 
usually no increase in meningismus. 

The presence of glucose, as shown by Fehling’s test, varies from the 


PROGNOSIS FOR OTITIC MENINGITIS 


391 


normal in certain diseases. There is usually a normal reduction by Feh- 
ling’s test in poliomyelitis and meningismus; it is diminished in a majority 
of cases of tuberculous meningitis. In meningococcic and purulent men¬ 
ingitis it may be normal at the onset and in very mild cases ending in re¬ 
covery may remain normal throughout the disease. In cases of average 
severity, however, the Fehling’s reduction is regularly diminished or absent 
as the disease reaches its height,—increasing in cases ending in recovery as 
convalesence is established. 

I wish to acknowledge my indebtedness for the above chiefly to Doctors 
DuBois and Neal. Their data, based on the results of seven years of work 
in the New York health board and on a correllation of the clinical and labor¬ 
atory findings in 1600 cases, are of a kind which should carry unusual weight. 
Among practical deductions drawn from this experience, may be mentioned 
the following. 

(1) Disappearance of sugar from the spinal fluid as shown by diminution 
or absence of the normal Fehling’s reduction is not a reliable early test of 
purulent meningitis, since in the majority of cases it is not present until 
the disease is well advanced. Since a return of the normal reduction often 
marks a turning point in the lesion for the better, repeated tests may furnish 
useful prognostic data. 

(2) In purulent and in meningococcic meningitis a high polymorphonu¬ 
clear percentage is a characteristic feature of the spinal fluid. A gradual 
and progressive increase in the relative number of the mononuclear cells 
is a frequent concomitant of a change for the better and is a good prog¬ 
nostic sign. 

(3) Progressive diminution of the albumen and globulin to a normal 
basis often keeps pace with a favorable change in the progress of the lesion. 

(4) Favorable changes in the chemical and physical properties of the 
spinal fluid— e.g., reduction of cell count, albumen and globulin, increase in 
sugar, etc.—without coincident disappearance of the pathogenic micro¬ 
organism, are unfavorable signs. Such cases usually end fatally. 

With regard to the isolation by smears or cultures of the causative micro¬ 
organism in the spinal fluid, a positive finding of course definitely classifies 
the lesion. A negative finding in fluid from the first or second puncture does 
not, however, necessarily indicate a non-purulent meningeal lesion since the 
germ may be isolated from a specimen obtained from a later puncture. 

Prognosis. —In speaking of the prognosis, one must necessarily take 
somewhat into account the various types of the disease, since in cases which 
recover the diagnosis is so often open to discussion, that purulent lepto¬ 
meningitis is not a hopelessly fatal disease may be considered proved by the 
large number of authentic and trustworthy case reports in which recovery 
has taken place. It is conceivable that a meningeal infection involving only 
a small area may produce all the characteristic clinical phenomena and 
release pyogenic micro-organisms into the spinal fluid ) and it is piobable 
such circumscribed lesions have furnished a large proportion of the recov¬ 
eries. Of the various micro-organisms which may reach the meninges from 


392 


INTRACRANIAL LESIONS OF OTITIC ORIGIN 


the ear, the streptococcus mucosus capsulatus (now regarded as identical 
with the pneumococcus no. 3) seems to be the most fatal, few recoveries 
having been reported, so far as the writer knows, in which this germ was 
found in the spinal fluid. 

Treatment.— It must be confessed that the surgical treatment of men¬ 
ingitis has not yet been placed upon a scientific basis. And yet, enough 
cases have been successfully operated upon to place upon the surgeon a 
grave responsibility in the treatment of cases. So far as a logical course of 
procedure may be formulated, it may be stated briefly as follows: 

If an otitic origin is in doubt, a lumbar puncture might give important 
data. There is little question that cases of meningitis of the epidemic, or 
meningococcic, type coexisting with aural suppuration, have in some cases 
been operated upon on the hypothesis of an otitic origin. A positive finding 
of the meningococcus in the spinal fluid would supply definite indications as 
to treatment: i.e., intraspinal administration of the antimeningitis serum, and 
no surgical intervention unless separately indicated for the mastoid lesion. 

In cases in which the spinal fluid is increased in quantity but clear and 
otherwise approximately normal, the question of a transitory meningismus 
must be taken into account. Operative treatment may be absolutely con¬ 
traindicated. On the other hand, it must be borne*in mind that not 
only pneumonia, intestinal infections and the acute infectious diseases, 
but also localized foci of infection, may cause the meningeal disturbance. 
Elimination of a suppurative process in the mastoid may, therefore, be 
called for. 

In cases of purulent leptomeningitis clearly traceable to an otitic origin, 
surgical treatment, to have any value, must not be delayed. Thorough 
removal of all diseased structures contiguous to the meninges is the first 
desideratum. This does not mean that time should be unduly expended 
upon the curetting of small sections of bone, but rather that diseased bone 
in contact with the dura should be freely removed in bulk, it being better to 
err in the direction of removing too much than of leaving necrotic or devit¬ 
alized bone in contact with the already hyperaemic or inflamed dura. This 
preliminary work upon the bone should be done with all reasonable rapidity, 
speed being an important factor in operations involving the brain or men¬ 
inges. 

In the treatment of meningitis, serous or purulent, the older view as to 
the necessity in all cases of incising the dura requires modification. We 
now know that in many cases of serous, and in some cases of purulent, 
meningitis thorough removal of diseased bone and free exposure of the ad¬ 
jacent dura are all that are required to bring about recovery. Usually the 
roof of the antrum and tympanic vault and contiguous portions of the 
squama are the parts to be removed. Generally speaking, the dura should 
be uncovered well beyond the boundaries of the area supposed to be in¬ 
volved. Cases of recovery following this procedure have been recorded by 
Brieger, Hinsberg, Gragenigo and others in Europe and have been observed 
by many surgeons, including the author, in this country. 


TREATMENT OF OTITIC MENINGITIS 


393 


Should symptoms of serous encephalitis be pronounced, or in any case 
should the operation above described not result in fairly prompt relief of the 
meningeal symptoms, there should be no delay in incising the dura. 

The macroscopic appearance of the exposed dura is not a reliable guide 
as to the presence or absence of a serous or purulent meningitis. Superficial 
congestion of the dura or even granulations thereon are often noted in cases 
in which all meningeal symptoms are absent, and, on the other hand, a 
dura of normal appearance may coexist with subdural oedema or actual 
infection. 

Where incision of the dura is indicated, the best results are probably 
obtained by two or more short incisions extending into the subarachnoid 
space or into the cerebral cortex. No attempt to introduce a wick or drain 
of any kind beneath the dura or into the brain substance should be made, 
simple incision providing the relief of tension and withdrawal of excess 
cerebral fluid which the operation aims to secure. 

While diffuse purulent leptomeningitis is probably a hopelessly fatal 
disease, it is not always possible to determine the diffuse character of the 
lesion from the clinical manifestations. I believe, therefore, that it is just¬ 
ifiable in every case to give the patient the advantage of operative inter¬ 
vention. Careful removal of all diseased bone and free exposure and in¬ 
cision of the involved area of dura constitute theoretically the best surgical 
treatment, and in certain cases not clinically distinguishable from diffuse 
leptomeningitis may bring about recovery. 

In the earlier years of his experience the writer saw several cases of 
otitic leptomeningitis treated by incision and attempted drainage by the 
introduction of small wicks of folded gauze or folded rubber tissue beneath 
the dura, but never one that did not end fatally. 

Lumbar Puncture for Relief of Pressure .—Lumbar puncture repeated 
at intervals for the purpose of relieving intracranial pressure has been 
more or less extensively advocated and practised in otitic meningitis. While 
certain cases in which it was used have recovered, there is no evidence 
that such favorable results have been to any extent attributable to the 

withdrawal of fluid from the spinal canal. 

Use of Drugs .—As to the internal administration of drugs,— i.e., either 
hypodermically or by mouth—there is not the slightest evidence that 
they exert any influence whatsoever on the course of the disease. 


CHAPTER XIV. 

BARANY’S THEORY OF CEREBELLAR CENTRES: NORMAL ACCURACY 

IN POINTING WITH EYES CLOSED: NORMAL REACTION MOVE¬ 
MENTS IN RESPONSE TO VESTIBULAR IRRITATION: LOSS 
OF POINTING ACCURACY AND CHANGES IN THE 
REACTIONS TO VESTIBULAR IRRITATION 
IN CEREBELLAR DISEASE. 

No discussion of the symptoms of cerebellar abscess would be complete 
without reference to the important work of Professor Robert Barany, now 
of the University of Upsala, in establishing the theory of cerebellar local¬ 
ization. According to this theory, there exist in the cerebellar cortex, 
certain centres which exert each upon some particular joint or its controlling 
muscle group, a pull, or tonus, in a certain direction. The influence of these 
centres does not, as in the case of the cerebral motor centres, control the 
voluntary movements of the muscle group or groups over which they pre¬ 
side. Rather they have to do with orientation, or the sense of position of 
different parts of the body with reference to certain fixed points in space. 

Each cerebellar centre exerts upon some particular joint or its control¬ 
ling muscle groups, a pull, or tonus, in a certain definite and constant direc¬ 
tion. For each joint there exists separate centres which maintain tonuses 
in different directions. There are, for example, separate centres which ex¬ 
ert respectively an inward and an outward tonus, or pull, upon the muscle 
groups of the shoulder. The operation of these two tonuses, acting in nor¬ 
mal balance or equilibrium, confers upon the individual the ability to move 
the arm in the vertical plane without the aid of sight. Logically in such 
a scheme there must be additional centres for each joint exerting respectively 
an upward and downward pull, to maintain correct orientation or move¬ 
ment in the horizontal plane. 

Apparently the cerebellar cortex contains four rather large areas, or 
centres, which may be thought of, not with reference to the joints they con¬ 
trol, but in accordance with the direction of the tonus, or pull, which they 
exert upon all the principal joints of the body. In other words, the separate 
centres exerting, for example, an inward tonus upon the various joints are 
contiguous, or at least in rather'close proximity to each other, the area in 
which they are grouped being spoken of as a direction centre. Thus, there 
are direction centres for inward, outward, upward and downward pull, or 
tonus, respectively. Within each direction centre are smaller centres spe¬ 
cialized for the different joints, e.g., shoulder, elbow, wrist, hip, knee, ankle, 
the neck, etc. 

As to the influence of disease upon one or any of these cortical cerebellar 
centres: let us take for an example the shoulder joint, in which the ability 
with eyes closed to move the arm correctly in the vertical plane depends upon 
394 


NORMAL POINTING REACTIONS 


395 


the proper and coordinated functioning of the two centres exerting respec¬ 
tively an inward and outward pull upon that joint. If, now, the centre for 
inward tonus is destroyed by surgical accident or disease, the arm no longer 
moves correctly in the vertical plane, but veers outward, being drawn thither 
by the unopposed force of the still intact centre for outward tonus. 

In order to convert this theory of cerebellar localization into a prac¬ 
tical working hypothesis, it will be necessary to pause here to state briefly 
certain facts and describe certain phenomena upon which the so-called 
pointing tests are based. 

Normal Pointing Accuracy. —The average normal individual with eyes 
closed and having located some fixed object by the sense of touch—say with 
the index fingei of either hand—can raise the hand and arm to the vertical 
or upright position and then bring the finger again into contact with the 
object touched, or will miss it only b} r a fraction of an inch. If, instead of 
raising the hand, the arm be moved in the horizontal plane so that the hand 
travels through one fourth of the arc of a circle, it can be brought back, 
again traversing the horizontal plane, to contact with the object touched. 
This represents the normal standard of accuracy. 

Method of Applying Pointing Test .—The pointing test most commonly 
employed is of the accuracy of movement in the vertical plane and is applied 
as follows: the examiner and patient stand or sit facing each other, the lat¬ 
ter with eyes blind-folded or closed and with the arm to be tested extended 
straight in front of him. The hand is pronated so that the palmar surface 
which is to receive the touch impression is directed downward. In contact 
with the palmar surface of the patient’s forefinger, thus extended, the ex¬ 
aminer places his own finger, pressing upward. The patient is now instructed 
to raise the hand and arm to the vertical (upright) position and then rather 
slowly lower his finger to contact with that of the examiner, which has been 
held immovably in the original position. The average normal individual 
finds no difficulty in doing this, or misses only by a fraction of an inch. 

Normal Pointing Reactions in Response to Vestibular Irrita- 

tion ._We are now in a position to study the character of the deviation 

from normal pointing accuracy which regularly accompanies sudden 
disturbance of either vestibular apparatus, either as a lesult ol disease oi 
of experimental stimulation. 

Mtthod of Applying Test .—If we irrigate with cold water, let us say, the 
right ear (patient’s head being held erect), there is developed a well-marked 
rotary nystagmus to the left, and the individual, attempting to stand, tends 
to fall to the right. Now quickly, i.e., while the nystagmus is still active, 
test his pointing accuracy in the vertical plane, first with one hand and then 
with the other, by the method above described. It will be found that, hav¬ 
ing located the examiner’s finger with his own, the hand in being raised will 
swerve somewhat from the vertical plane to the right, and again in being- 
lowered will deviate further to the right. His hand, then, in being elevated 
and depressed describes an inverted V falling to the right of the object he is 
trying to reach. Stating this in the form of a rule, we may say that the point - 



396 BARANY’S THEORY OF CEREBELLAR CENTRES 


ing deviation resulting from vestibular irritation is invariably in the direction 
opposite to that of the induced nystagmus. It therefore corresponds with the 
direction of the falling tendency,— i.e., with the direction in which, if he 
attempted to stand, he would demonstrate a tendency to fall. In a normal 
person these reactions are present in both arms. 

Changes in Pointing Accuracy in Cerebellar Disease. —Like 
other focal symptoms of cerebellar disease, changes in pointing accuracy 
may or may not be present. When present, they may be the deciding factor 
in an otherwise obscure case. Their absence, however, is no indication that 
the cerebellum is not diseased. 

Application of Test .—The patient, being blind-folded or with eyes closed, 
the pointing accuracy of the two arms is separately tested by the method 
already described, in a case of cerebellar abscess in which the centre for 
inward tonus upon the shoulder is involved, it will be found that the arm 
corresponding to the cerebellar lesion will deviate outward while the oppo¬ 
site (i.e., that corresponding to the sound side) will continue to point with 
normal accuracy. Thus in a lesion of the right cerebellar hemisphere, the 
right hand deviates outward, i.e., to the right; with a left cerebellar lesion, the 
left hand deviates to the left, the arm corresponding to the sound cerebellar 
hemisphere maintaining in either case the normal pointing accuracy. This 
is the first part of the test. We must now confirm the result thus ob¬ 
tained by testing the reaction to vestibular irritation. 

Supposing, for example, that in a case of suspected cerebellar abscess we 
have tested the pointing accuracy of both arms and found that the right 
shows unmistakable outward deviation (i.e., to the light) while the left arm 
points accurately,—this, so far as it goes, would indicate disease of the right 
cerebellum. We must now test the reaction of the right arm to vestibular 
irritation. This is done by irrigating the left ear (i.e., ear of opposite side to 
the supposed lesion) with cold water. This is followed by a rotary nystag¬ 
mus to the right, during which in a normal individual both hands in point¬ 
ing would deviate strongly to the left. If now in the presence of an induced 
nystagmus to the right, the right arm does not deviate as normally to the 
left, but continues as formerly to deviate to the right, while the left arm 
shows the normal reaction to the left, we have a clear and positive indica¬ 
tion of a lesion involving the right hemisphere of the cerebellum. 

In order to illustrate these reactions, it may be well, though many typ¬ 
ical cases have since been reported, to cite only two or three of the classical 
cases given by Professor Barany in his original reports. 

Case I.—This patient, a boy, exhibited some of the general symptoms 
suggesting an intracranial suppurative lesion, but (excluding pointing tests) 
no focal or localizing symptoms pointing to cerebrum or cerebellum or in¬ 
dicating in which side of the skull the lesion, if present, should be looked for. 
The pointing tests demonstrated the following conditions: The left arm 
maintained its normal pointing accuracy, and in response to vestibular 
irritation showed normal reactions. The right arm, on the other hand, ex¬ 
hibited constant spontaneous outward deviation, i.e., to the right. When 


CEREBELLAR CENTRES 


397 


the left ear was irrigated with cold water, the usual rotary nystagmus to the 
right was induced, but the right hand did not show the normal deviation 

to the left. 

On these two functional changes,—viz., spontaneous outward deviation ot 
the right arm and its failure to respond as normally to vestibular irritation, a 
diagnosis of right cerebellar abscess was made. This diagnosis was confirmed 
by an operation during which the abscess was located and evacuated. 

Let us now note in this case the further functional changes which fol¬ 
lowed the opening and evacuation of the abscess. Two days after the opei- 
ation it was found that the pointing accuracy of both arms was normal,— 
or, in other words, the spontaneous outward pointing deviation of the light 
arm had entirely disappeared. When, however, the reaction to vestibular 
irritation was tested, it was found that when the left ear was irrigated with 
cold water, the left arm showed the normal deviation to the left, while the 
right arm continued to point with normal accuracy. In other words, as a 
result of the cerebellar abscess or quite possibly of the incision through 
which it was evacuated, the right arm could no longer be made to deviate 

to the left in response to vestibular irritation. 

Since Cases II and III (also from Barany’s original reports) are cited 
chiefly for their bearing upon the position of certain centies, a biief di¬ 
gression to define their location may serve a useful purpose. As the cases 
Trom which our knowledge has been chiefly derived are for the most part 
those of cerebellar abscess of otitic origin, it is clear that the cerebellar 
surface extending from the anterior border of the sigmoid sinus forward 
alono- the posterior aspect of the petrous bone to the internal auditoi\ 
meatus represents the general area which should first be investigated; 
and it is a fact that in the cases in which these phenomena have been 
most clearly demonstrable, the lesion has usually been found m close 

proximity to this area. i 

Cerebellar Centres for Wrist and, Shoulder (Fig. 196).—Barany places the 
centre exerting an inward tonus, or pull, upon the wrist joint in the anterior 
end of the middle inferior lobe (slender lobe)—that portion of it which is 
nearest the flocculus (1). The centre exerting a similar tonus upon the 
shoulder joint is located also in the middle inferior lobe, but behind the 
wrist centre by about 10 or 12 mm. (2). The evidence as to the correct 
localization of these two centres will be stated presently. _ The centre 
exerting a downward pull upon the shoulder joint, destruction or severe 
injury of which would cause pointing deviation upward, is placed in the 
most superior and inner corner of the hemisphere, and includes adjacent 
surfaces of the superior and inferior semilunar lobes The centre for outwaid 
tonus (shoulder joint) is located in the outer or lateral margin ot the lobus 

semilunaris superior (3). , , t u p 

Of these centres the first two (those exerting inward tonus upon the 

wrist and shoulder movements respectively) are by far the most 

from the standpoint of practical diagnosis for the reason that they ate - 

centres most commonly involved in cerebellar lesions ot otitic origin. 


398 BARANY’S THEORY OF CEREBELLAR CENTRES 


In cases of cerebellar disease in which spontaneous pointing deviation 
has been present, various joints have quite frequently been demonstrably 
involved,— e.g., shoulder, elbow, wrist, hip, knee, ankle; also the neck and 
the trunk as a whole. A careful investigation of the different joints will 
therefore prove of academic interest, and in the case of small and slowly 
growing tumors may be of very practical diagnostic importance. I am 
inclined to believe, however, that in any case of otitic cerebellar abscess in 
which the arm and wrist show no spontaneous pointing deviation and in 
which the vestibular reactions are normal, little of practical advantage will 
be gained from the investigation of other joints. 

Evidences of the Correct Localization of Centres for the Wrist and Shoulder 
(inward tonus).—As bearing upon this point, two more cases from Barany’s 
reports may be cited. 

Case II.—In a case operated upon in the Vienna General Hospital the 
cerebellar dura in front of the sigmoid sinus had been freely exposed. Dur¬ 
ing the further course of the operation an instrument in the surgeon’s hands 
slipped, entering the cerebellum through the middle inferior lobe near the 
flocculus. After recovery from the anaesthetic, his pointing accuracy was 
tested. The wrist corresponding to the side of the surgical mishap deviated 
strongly outward, the opposite hand and arm pointing accurately. 

Case III.—Patient in this case presented certain general features of 
cerebellar abscess, but no focal symptoms. Exploratory operation was 
decided upon. First one cerebellum and then the other was explored, no 
abscess being found on either side. On each side an exploratory puncture 
was made through the slender lobe at the point located as the centre for 
the shoulder joint (inward tonus). The case therefore furnished a unique 
opportunity of corroboratory tests. After recovery from the anaesthetic, 
pointing tests were made. Both arms showed very marked and character¬ 
istic deviation outward. 

Effect of Freezing .—As further evidence, Barany made use of several 
cases of patients who had recovered from operations leaving extensive 
dural areas in front of the sigmoid sinus uncovered, or covered only by a 
thin layer of skin. The experiment was repeatedly carried out by freezing 
by means of an ethyl chloride spray the centre for the shoulder (inward 
tonus). It has been found that after freezing this centre for a period of 2 l /> 
minutes, strong outward deviation has invariably been established. 

While I have made use of Barany’s cases to illustrate a set of phenomena 
the discovery of which was wholly the product of his brain and years of 
study, I have seen many cases in which these particularly useful focal sjmip- 
toms were present. In one case which I saw with another surgeon, the pa¬ 
tient who had been operated upon for mastoiditis, exhibited certain vague 
symptoms suggestive of intracranial involvement. A tentative diagnosis 
of “a low form of meningitis” had been made. The pointing tests showed 
well marked outward deviation confined to the right hand, and an operation 
the same day located and evacuated a right cerebellar abscess, the patient 
making a good recovery. 



Fig 196.—Inferior Surface of Encephalon. (1) Centre for inward tonus (wrist \ 
for inward tonus (shoulder). (3) Indicates position on superior semilunar lobe ot the 
outward tonus, or pull, on the shoulder joint. 


(2) Centre 
centre for 


















CHAPTER XV. 

SURGICAL OPERATIONS FOR THE RELIEF OF SUPPURATIVE LE¬ 
SIONS OF THE MIDDLE EAR AND MASTOID PROCESS; 

myringotomy; mastoidectomy; the radi¬ 
cal operation; ossiculectomy. 

myringotomy; incision of the drum membrane; paracentesis. 

There is probably no one surgical procedure which has been the means 
of saving a larger number of lives than the judicious evacuation of pus from 
the tympanum through an incision of the drum membrane. It may be said 
to be positively indicated in every case of suppurative otitis media in which 
the drum membrane is found to be displaced outward (bulging) by pressure 
of confined pus. Reducing this statement to more exact terms, we recog¬ 
nize the following conditions calling for incision of the drum membrane: 




Fia. 197. 


r'XG. 198. 



Fig. 199. 


Fig. 200. 



Fig. 197.—Incision indicated in a suppurative lesion confined to the atrium. 

Fig. 198.—Incision indicated in suppurative lesion involving the tympanic vault. 

Fig. 199.—Incision supplementing inadequate perforation. 

Fig. 200.—Incision occasionally indicated in chronic suppurative otitis media for the evacuation 
of pus retained in the vault. 


1. Acute purulent otitis media confined to the atrium, as shown by 
bulging of the membrana tensa as a whole (Fig. 197). 

2. Acute purulent otitis media involving the tympanic vault, as shown 
by bulging of Shrapnell’s membrane and the upper posterior segment of 
the tense membrane (Fig. 198). 


399 














400 


TYMPANIC AND MASTOID OPERATIONS 


3. Suppurative otitis media with resolution delayed by the insufficient 
drainage provided by a small and inadequate perforation (Fig. 199). 

4. Subacute otitis media characterized by an inflamed and infil' 
trated drum membrane and the presence of fluid—serum or pus—in the 
lower half of the atrium. 

5. Acute exacerbation of chronic suppurative otitis media, with per¬ 
foration or loss of membrana tensa and physical signs of pus retention in 
vault (Fig. 200). 

Operative Dangers. —The surgical accidents occasionally reported 
as resulting from the abnormal position of important structures— e.g., 
division of an exposed facial nerve, injury to an abnormally placed and 
exposed jugular bulb, etc.—are surgical dangers which are mentioned in 
most text-books. They depend upon exceedingly rare conditions which 
can not be allowed for by the physician. Of more serious import to the 
surgeon, because due solely to his error or carelessness, is the production 
of a surgical injury leading to suppurative labyrinthitis. Holinger has 
recorded a case in which the patient, suffering from acute purulent otitis 
media of the right ear, experienced severe dizziness immediately following 
a myringotomy. The vertigo and ataxia suggested labyrinthine disease 
and were so great as to confine him to bed. The symptoms of suppurative 
labyrinthitis rapidly gave place to those of meningitis, from which disease 
the patient died. Post-mortem examination showed fracture of both 
crura of the stapes and rupture of the capsular ligament, leaving the 
vestibule open to infection. To this case the writer can add one which 
came under his observation. The patient, a man of thirty whose hearing 
had previously been perfect, suffered an attack of acute middle-ear inflam¬ 
mation with the usual accompanying earache. He called upon a physician, 
who incised the drum membrane. Immediately following this operation, 
the patient experienced very severe dizziness and was obliged to go to bed. 
During the next ten days he was confined to bed by vertigo, nausea, and 
vomiting, at first severe but showing a gradual diminution. When I first 
saw him the drum membrane had healed but was still much congested. 
The right ear was absolutely deaf for all sounds. There was no caloric 
reaction. Apparently this was a case of traumatic infection of the laby¬ 
rinth, from which the patient had recovered with absolute loss of function. 
Dr. John R. Page has informed me of a similar case which came under his 
personal observation. How often such accidents have actually occurred 
there is no means of determining. The important fact is that they do occur 
and that they are preventable. I am inclined to believe that the stapes or 
region of the oval window furnishes the usual point of attack, and that the 
injury is in most cases the result of a lack of exact knowledge or appreciation 
of tympanic anatomy rather than of a rough or careless use of instruments. 

It will be remembered that neither the drum membrane nor the inner 
tympanic wall is in a plane at right angles to the long axis of the bony 
meatus. The drum membrane, for example, is very obliquely placed, 
forming decidedly obtuse angles with the roof and posterior wall of the 
bony meatus, and very acute angles with its floor and anterior wall. The 


INCISION OF DRUM MEMBRANE 


401 


inner tympanic wall likewise is directed from above downward and strongly 
inward, so that it also forms an obtuse angle with the plane of the roof of 
the bony meatus and an acute angle with 
that of its floor (Fig. 201). These facts are 
restated and emphasized with the purpose 
of enforcing a point I wish to make,—viz., 
that the incision of the drum membrane 
should in every case begin below and be ex¬ 
tended upward, and never in the reverse 
direction,— i.e., beginning above and ex¬ 
tending downward toward its lower margin. 

It will be recalled that in incising an 
intact but bulging membrane the incision 
is practically always made through its pos¬ 
terior segment. If now we essay to make 
our incision from above downward, and 
plunge the knife through a point at or near 
its upper margin, with the cutting edge 
directed downward, we shall be likely to 
forget the normal slant of the membrane, 
and find later that the knife has quickly 
cut its way out, making only a short 
and totally inadequate incision (Fig. 202). 

Keeping the oblique plane of the drum membrane in mind, it is, of course, 
possible to obviate this error by carrying the knife simultaneously down- 



v 
I 


Fig 
external 
cavity. 


201.— Vertical section through 
auditory canal and tympanic 



Fig. 202.—Diagram showing technical 
error likely to result from an incision made 
from above downward. 



Fig. 203.—Diagram showing double 
movement (i.e. downward and inward) 
required in incising the membrane 
from above downward. 


ward and inward, so that it emerges from the drum membrane only at 
its lower margin (Fig. 203). But in trying to execute this rather difficult 
26 















402 


TYMPANIC AND MASTOID OPERATIONS 


movement there is some danger that we may carry the point of the knife 
too far inward at the start, and, in the case of a low and prominent 
incudostapedial articulation, engage this or even the crura of the stapes, 
and with the downward stroke either drag the stapes altogether out of the 
oval window or at least produce a rupture of its capsular ligament, thereby 
admitting pus into the cavity of the vestibule (Fig. 204). If, on the other 
hand, we begin at the lower margin of the membrane and bear in mind 
its oblique plane, we can make the incision while withdrawing the knife. 



Fig. 205.—Incision of drum mem¬ 
brane from below upward, the correct 
method. 


Fig. 204.—Dangerous accident (sta¬ 
pedial dislocation) which may result 
from an incision from above downward. 


Cutting in this way, the point of the knife is moved constantly away from 
danger points; and with ordinary care we are in no great danger, even 
though we may touch the incudostapedial joint, of producing serious 
injury or traumatism (Fig. 205). 

Injury of the Chorda Tympani Nerve. — This is an occasional acci¬ 
dent resulting from an extensive incision of the drum membrane. It 
probably occurs oftener than either the physician or the aurist knows. 
It is announced altogether by subjective symptoms, — i.e., the patient 
experiencing a sensation of numbness, and also losing the sense of taste 
on the side of the tongue corresponding to the ear incised. Whether 
the division of the nerve is usually complete or only partial, the resulting 
disturbance is, as a rule, short-lived. The symptoms referred to have 
occurred several times in the writer’s experience, but have never seemed 
to disturb the patient greatly, and have always disappeared, or at least 
ceased to attract the patient’s attention, within a few weeks. 

Preparation for Operation. —The preparation of the patient is 
simple. The auricle if obviously unclean should be scrubbed with soap 
and water and dried. With the patient lying with the diseased ear directed 









INCISION OF DRUM MEMBRANE: TECHNIC 


403 


upward, the canal is filled with peroxide of hydrogen, which should be 
allowed to remain four or five minutes. The ear is then irrigated with a 
warm solution of bichloride of mercury, 1 in 2000, or carbolic acid, 1 in 200. 
A full quart of the solution should be allowed to flow in and out of the ear 
from a fountain syringe. The canal is then lightly packed with sterile 
gauze or cotton. This completes the preparation of the operative field. 

The instruments, consisting of aural specula, cotton applicators, and 
bayonet forceps, are cleansed by boiling, the knife-blade being immersed 
first in strong carbolic acid and then placed in alcohol. As to the prepa¬ 
ration of the hands, I prefer simply to wash them thoroughly with soap 
and water, then arrange my head-light or mirror, and at the last minute— 
i.e., just as the patient is passing under the influence of the anaesthetic— 
to draw on a pair of previously sterilized rubber gloves. 

Anaesthesia. —I believe very strongly that unless there are positive 
contra-indications the patient should be under the influence of a general 
anaesthetic. For this purpose nitrous oxide is an ideal drug. It acts 
quickly, is easily prolonged to the time required for a double myringotomy, 
—or longer if necessary,—and usually leaves the patient without any 
sense of discomfort referable to its administration. Aside from the saving 
of unnecessary pain to the patient, it enables the physician to make his 
incision with exactness and precision, which is not always possible without 
anaesthesia. In the case of children the use of a general anaesthetic is even 
more important, since, if it is omitted, the little patient may conceive a fear 
of the physician which will render all subsequent treatment most difficult. 

Local Anaesthesia .—I know of no efficient local anaesthetic appropriate 
to this operation. A solution containing cocaine and carbolic acid in the 
strength of 10 per cent, of each is quite efficient in some cases, in others 
seeming to have comparatively little influence upon the pain. It is applied 
by saturating with the solution a small pledget of sterile absorbent cotton 
which is placed in contact with the drum membrane and allowed to remain 
not longer than two minutes. The use of stronger carbolic solutions has 
been advised, and naturally may be counted upon to act with greater 
certainty upon the sensory nerves of the part. But they are to be con¬ 
demned as subjecting the drum membrane to very considerable risk in 
the destructive processes which not infrequently follow the local use of 
carbolic acid in strong solutions. 

Technic. —Before attempting this delicate and very important little 
operation, the student should have a clear appreciation of the mechanical 
results which he wishes to achieve. We no longer speak of “puncturing” 
the drum membrane, because we now know that the most extensive incision 
which the lesion permits will be none too long for perfect drainage and, while 
affording better and more permanent relief of symptoms, will eventually 
heal quite as readily, and perhaps more perfectly, than a smaller opening. 

Having determined upon the extent and direction of the incision, we 
should endeavor to carry this into effect without injury to other tympanic 
structures. In other words, if our aim is to drain the tympanum through 


404 


TYMPANIC AND MASTOID OPERATIONS 


an opening in the drum membrane, we should endeavor to confine our 
incision to the drum membrane. The contention of Dench, 1 that we should 
incise not only the drum membrane but also the inflamed mucosa cover¬ 
ing the inner wall, is open to the following objections, viz., (1) To in¬ 
cise voluntarily a congested mucoperiosteal membrane covering the bony 
wall of a pus-filled cavity opens the way to possible pathways of infection 
which may lead to regions beyond our surgical control {e.g., to labyrinth 
or meninges). (2) To cut with the kmfe-pomt in contact with the inner 
tympanic wall is to incur risks of injury to the labyrinthine capsule, 
e.g., stapes, capsular ligament, or at some point of erosion upon the prom¬ 
ontory. Such an injury might easily lead to suppurative labyrinthitis. 

It is assumed that the physician will have gained some facility in the 
manipulation of instruments,— i.e., with probes, cotton applicators, etc., 
before attempting to use the myringotomy knife. The knife is most easily 
controlled if held between thumb, index and middle fingers, much as we 
hold a pen in writing (Fig. 206). The commonest types of failure are those 



in which the incision is either (a) not in the drum membrane, or (b) not 
so placed as to insure the most perfect drainage. Neither of these acci¬ 
dents is particularly uncommon with beginners. Failure to include any 
portion of the drum membrane in the incision is obviously due to the 
operator’s failure to recognize normal landmarks or, these being obscured, 
failure to distinguish between the bulging drum-head and the contiguous 
swollen canal wall, so that on his next inspection of the ear he finds the drum 
membrane still bulging or spontaneously ruptured, and is able to distinguish 
the line of his incision in the posterior wall of the canal. This mortifying 
experience has occurred to many a beginner in otology and is perhaps a 
wholesome one in bringing home to him the importance of a careful study 
of the small operative field before using the knife. This particular accident 


1 Dench: Diseases of the Ear, 1904, p. 487. 















INCISION OF THE DRUM MEMBRANE 


405 


is likely to occur only in those cases in which the bulging posterior segment 
of the drum-head merges without any distinguishable line of demarcation 
into the swollen posterior canal. It is avoided by a careful search for the 
hammer handle, which, though frequently obscured, can usually be located 
by a slight linear depression along the line of its attachment to the drum 
membrane. Having recognized, or at least determined the position of the 
hammer handle, our incision should in these cases be not more than 1 or 
\ l /2 mm. behind it. 

The second and commonest error— i.e., of an improperly placed in¬ 
cision—is probably more often due to imperfect control of the knife than 
to a lack of knowledge as to where the incision should be made. I believe 
that these failures are oftenest explained by the surgeon’s failure to intro¬ 
duce the knife at the correct point upon the drum membrane. He sees the 
point which he wishes to represent his initial puncture, but fails to strike 
it with the point of his knife. The cause of this deviation is probably anal¬ 
ogous in many cases to swerving of a pistol in the hands of a beginner at 
the time he pulls the trigger. Once the knife is improperly introduced, 
the remainder of the incision is necessarily thrown out of its correct course, 
though the operator may be blinded to this defect by the resulting hemor¬ 
rhage until the patient has come from under the influence of the anaesthetic. 
If the operation has for any reason been performed without the aid of a 
general anaesthetic, it will be usually quite impossible to correct any error 
in one’s initial incision. It is expecting too much of the patient to require 
him to endure the torture of a second incision in so exquisitely sensitive a 
structure as the inflamed drum membrane. 

It will be seen from the above that the author has endeavored to sug¬ 
gest the commoner types of failure, their causes, and the means by which 
they may be avoided, rather than to describe in detail the steps of the 
operation. Assuming that the physician possesses a practical knowledge 
of the drum membrane and its tympanic relations, and that he knows 
where the incision should be made, I believe that there are only three 
essentials to his acquiring quickly a satisfactory technic in this \ei\ im¬ 
portant little operation,—viz., (1) he should insist upon having his patient 
under the influence of a general anaesthetic; (2) he should carefully and 
without haste bring the point of his knife, with cutting edge directed up¬ 
ward, to the point which he wishes to represent the lower end of the in¬ 
cision; and (3) he should extend the incision upward without haste and 
always under the guidance of sight, i.e., without at any moment losing 
sight of the line of his incision. 

3 Removal of Post-over alive Clot— Following a myringotomy there is 
always a moderate hemorrhage into the canal, and, unless this receives 
attention, the purpose of the operation may be defeated by the resulting 
clot, I, personally, like to wait about ten minutes and then syringe the 
ear with a warm solution so as to see for myself the expulsion of the coagu¬ 
lating blood. If the first irrigation is too long delayed and then imper¬ 
fectly carried out by the nurse or attendant, it is possible that the clot may 


406 


TYMPANIC AND MASTOID OPERATIONS 


not be dislodged and may partially or completely seal the incision, pre¬ 
venting the drainage of the infected cavity which was the chief end in 
view. I have known this actually to occur. The initial clot having been 
removed, there is usually no recurrence. 

Possible Repetitions. —It must be remembered that one of the charac¬ 
teristic features of the normal drum membrane is its remarkable tendency 
to rapid healing after incision or accidental puncture, provided infection of 
the tympanic cavity does not take place. This tendency occasionally acts 
disadvantageously in cases of purulent otitis media, quick partial healing 
interfering with the free drainage which the incision was intended to secure. 
When this occurs, there should be no hesitation as to repeating the opera¬ 
tion. I have known cases in which the judicious repetition of this lesser 
operation has undoubtedly saved the patient from the severer ordeal of a 
mastoid operation. 

% 

SURGICAL LANDMARKS OF THE MASTOID CORTEX. 

Probably in no region of the body outside of the skull do so many 
important structures so nearly approach each other as in the body of the 
temporal bone. Here, within a space little more than half an inch square, 
are found the essential organ of hearing, the semicircular canal system and 
vestibular apparatus, the cochlear and vestibular branches of the auditory 
nerve, and the horizontal portion of the facial nerve. Injury to any one 
of these structures must inevitably cause either grave functional disorder 
or actual deformity. A little more than half an inch from any of them, we 
come upon the thin bony coverings of the sigmoid sinus, the bulb of the 
jugular vein, the brain, or the cerebellum. Clearly it is a region in which 
the surgeon should know his ground. 

There are two sets of surgical landmarks with which it will repay the 
student to become familiar before attempting to operate upon the living 
subject,—viz., (1) those upon the outer surface of the mastoid cortex which 
enable him to determine approximately the positions of important struct¬ 
ures beneath; and (2) those encountered within the bone during operation 
which indicate the exact location of structures he may wish either to 
attack or to avoid. 

Before describing the various operations, it may be worth while to 
consider brieflv the surgical landmarks of the outer surface of the mastoid 
(Fig. 207). 

The Suprameatal Spine ( Henle’s Spine ).—At the point where the upper 
posterior wall of the bony meatus terminates or merges into the outer 
surface of the mastoid, is a crescentic bony spine (Fig. 207, a) known as 
the suprameatal spine, or spine of Henle. It is absent in the new-born, 
but is usually developed early in child life and is a very constant landmark 
in the adult. The centre of this spine marks fairly accurately—passing 
from without directly inward—the position of the floor of the ciditus ad 
antrum. 


SURGICAL LANDMARKS 


407 


It will be recalled that the antrum and tympanic vault are in reality 
but a single cavity, the antrum representing the posterior end of the tym¬ 
panic vault. The division of the antrotympanic cavity into two portions— 
i.e., the vault or attic in front and the antrum behind—is brought about 
by a central constriction known as the aditus ad antrum. The aditus is, 



Fig. 207. —Surgical landmarks of mastoid cortex: o, spine of Henle; b, posterior root of zygoma; 
g, temporal ridge; c-d, line representing direction of horizontal portion of facial canal; e-f, line 
indicating course of descending portion of facial canal. 

therefore, not a narrow passage, as described in some of the earlier text¬ 
books, but a triangular space of considerable size. The position of the 
floor of the aditus in relation to the outer mastoid cortex is indicated by 
the centre of Henle’s spine. This surgical guide is of practical value in 
certain cases in which the antrum is abnormally small. 

Posterior Root of Zygoma— Beginning anteriorly in the sharp upper 
edge of the zygoma, and running backward and usually more or less up¬ 
ward upon the squama, is a usually well-defined ridge, which forms part of 
the temporal ridge. That part of the temporal ridge which is just above 
the bony meatus and spine of Henle is known as the posterior root of 
the zygoma (Fig. 207, b). 

In mastoid surgery the posterior root of the zygoma is a useful and 
important landmark as denoting the level of safety above which one may 
in certain temporal bones enter not the antrum, but the middle fossa of 
the skull. The rule, therefore, should be to begin one’s initial opening 
well forward,— i.e., a little behind the spine of Henle,—and below the level 
of the posterior root of the zygoma. In observing this rule, one must bear 






408 TYMPANIC AND MASTOID OPEKATIONS 

in mind that the temporal ridge often curves upward upon the squama to a 
level considerably above that of the floor of the mid-cranial fossa. The 
level of safety is illustrated in Fig. 208 by the dotted line a-b, between 
which and the temporal ridge is a triangular space (c), through which one 
might easily enter the brain cavity. 


Fig. 208.—Level of safety in opening mastoid. The line a-b is a horizontal extension backward 
of the posterior root of the zygoma. Between this line and the posterior upward extension of the tem¬ 
poral ridge is found in many bones a point, c, through w'hich the chisel would enter not the interior 
of the mastoid, but the mid-cranial cavity. The line a—b represents, therefore, the level of safety. 



Course of the Horizontal and Vertical Portions of the Facial Canal .— 
While the facial nerve is deeply situated, and therefore liable to exposure 
and direct injury only in the depth of an operative wound, it is to some 
extent subject to injury by concussion or transmitted force, and may 
therefore be endangered by careless surgery in the simplest operation upon 
the mastoid. 

The ‘‘horizontal” and “vertical” portions of the facial canal are not 
exactly horizontal and vertical in direction. If we will imagine a line, 
more or less horizontal in direction, which passes through the centre of the 
spine of Henle, its anterior extension forming an acute angle of about 15 
degrees with the upper margin of the zygoma (Fig. 207, c-d), this will 
indicate fairly accurately the direction upon the inner tympanic wall of 
the horizontal portion of the facial canal. Again, imagine a line, approach¬ 
ing the vertical in direction, which passes through the centre of the supra- 
meatal spine above and is in contact with the anterior margin of the 
mastoid below (Fig. 207, e-f), and we shall have a fairly accurate guide 
to the course of the descending portion of the facial canal, from its bend, 
or knee, j ust beneath the floor of the aditus to its termination in the stylo¬ 
mastoid foramen. 


% 


I 







Fig. 210.—Instruments called for in any surgical operation 




























Fig. 211.—Self-retaining retractors. 


a, Kerrison’s retractor; b, Allport’s retractor. 



Fig. 212.—Langenbeck’s periosteal elevator 






























A-Fig. 213.—Large grooved chisel, or gouge 
Z?— Fig. 214.—Whiting’s gouge. 

C-Fig. 215.—Whiting’s gouge. 


Z)-Fig. 216.—Jansen’s chisel. 
Z?-Fig. 217 —Jansen’s chisel. 
F-Fig. 218.—Mastoid mallet 










































mmm 




Fig. 219.—Mastoid rongeurs 



PREPARATION OF THE PATIENT 


409 


mastoidectomy; the mastoid operation; sometimes called 

“schwartze’s operation.” 

For a chronological account of the gradual development of this im¬ 
portant operation, the reader is referred to the historical sketch in Whit¬ 
ing’s book on the mastoid operation. 2 For practical purposes it will suffice 
here to record briefly the succeeding steps in the evolution of the operation 
as practised to-day. (1) The first operations for the relief of suppurative 
mastoiditis of which we have authentic accounts were performed in the 
early half of the eighteenth century, and were undertaken chiefly for the 
evacuation of confined pus. The surgeon therefore contented himself with 
drilling a hole through the mastoid cortex; and, as this provided neither 
adequate drainage nor removal of diseased bone, a majority of patients 
died, and the operation fell justly into ill repute. (2) The next operation, 
still in the nature of a trephining operation, aimed to provide freer drain¬ 
age and incidentally to remove such bone as was obviously diseased. 
This marked an advance, but still failed by its results to establish the 
procedure as one of universally recognized usefulness. (3) Finally, in 1873, 
Schwartze 3 advocated and de¬ 
scribed a systematic method 
of removing the mastoid cor¬ 
tex, breaking down the mastoid 
cells, and providing at once 
free drainage from all infected 
spaces within the mastoid. 

This work of Schwartze laid 
the foundation upon which has 
been built up our modern 
system of aural surgery, and 
explains the fact that the 
simple mastoid operation is 
often spoken of as “Schwartze’s 
operation.” 

Preparation of the Pa¬ 
tient. —The side of the head 
should be shaved over an area 
measuring fully three inches in 
all directions from the auditory 
meatus of the diseased ear 
(Fig. 209). The meatus should 
be irrigated with a solution of 
bichloride of mercury, 1 in 2000, and lightly packed with sterile gauze. 
The parts are then scrubbed with soap and water, thoroughly dried, and 
a covering of sterile gauze applied. -These preliminary steps should 

2 Whiting: Modern Mastoid Operation, Blakiston, pp. 13 to 29. 

3 Schwartze: Arch, fur Ohrenh., Bd. ii, 1873. 



Fig. 209.—Area shaved for mastoid operation. 





410 


TYMPANIC AND MASTOID OPEKATIONS 



Fig. 220.—Mastoid curettes. 







































































MASTOID INSTRUMENTS 


411 



Fig. 221.—Richards’s mastoid curettes, 









































412 


TYMPANIC AND MASTOID OPERATIONS 


precede the operation by several hours. When the patient is on the 
table and under the influence of the anaesthetic, the shaved area and 
the auricle, both anterior and posterior surfaces, are painted with 
tincture of iodine. This provides rapid and perfect sterilization. A com¬ 
mon practice is to wipe the painted surfaces, just before the initial 
incision, with sterile cotton soaked in alcohol. This removes the 
iodine stain and perhaps lessens the risk of skin irritation, but 
whether it is wise, i. e., from the viewpoint of dependable asepsis, is 
open to question. 

When tincture of iodine is to be employed in an emergency case in 
which all the preparations are made when the patient is on the table, 
the shaved area should be rubbed vigorously with dry cloths, and the 
tincture of iodine immediately painted thereon. Any superfluous use of 
water and antiseptic solutions just before the iodine is applied is known 
to interfere with the bactericidal action of the latter. The iodine alone 
provides complete sterilization. 

The surgeon’s hands are prepared in accordance with general surgical 
rules which need nob be stated here. In addition to a very thorough 
cleansing with soap, water, and brush, and immersion for a minute or 
two in 1 in 2000 bichloride solution, the writer believes that there is dis¬ 
tinct advantage in the use of rubber gloves which can be subjected to more 
drastic sterilization than can possibly be applied to the hands. 

Instruments. —The instruments required for a mastoid operation 
may for convenience be thought of as belonging to two groups,—viz., 
(1) those in common use in any operation, — e.g., scalpels, artery-clamps, 
thumb forceps, scissors, ordinary retractors, needle-holders, etc.,—and (2) 
instruments especially designed for mastoid or bone surgery. It is so im¬ 
portant that these latter should be of correct design that the writer has 

had cuts made from photographs 
of those which in his own practi¬ 
cal experience have proved most 
satisfactory. 

In addition to the above, it is 


always well to have a set of ear 
specula, cotton applicators, and a 
myringotome in readiness, as it is 
frequently necessary to incise the 
drum membrane at the time of the 
mastoid operation; and it is only 
by including these tympanic tools 
among our mastoid instruments 
that we can be sure of having 
them when they are required. 
Position of Patient on Table.— The patient lies on his back, with 
head turned so that the diseased ear is directed upward. The head rests 
upon a sandbag or, better, upon a specially-designed wooden head-rest 
(Fig. 222), which is wrapped in sterile towels, and which prevents unnec- 



Fig. 222. 


-Wooden head-rest, or block, for use in 
mastoid surgery. 



EXPOSURE OF TLIE CORTEX 


413 


essary movement. The towels about the head are so arranged as to leave 
the face fully exposed to the view of the anaesthetist, who sits at the side 
of the table to which the face is turned. The ancesthetist should watch for 
unilateral facial twitching , which usually announces any surgical injury or 
even irritation of the facial nerve . Such danger signals should be at once 
reported to the surgeon. 

The Initial Incision (Fig. 223). —The initial incision should begin 
at, or just below, the tip of the mastoid ( b ) and be carried upward, parallel 
with, and one-quarter of an inch behind, the posterior line of auricular 



Fig. 223.—Initial incisions for exposing the mastoid cortex. 


attachment, to end at a point above the upper attachment of the pinna 
(a). In its lower two-thirds it should divide all structures down to the 
bone, but in the upper third the pressure should be reduced so as not to 
include the temporal muscle. While many surgeons divide the muscle 
throughout, it is rarely necessary to do so. If from the temporal ridge, 
to which the muscle is attached, the tissues are divided only down to the 
surface of the muscle, the anterior skin flap can be easily deflected from it 
so as to permit the necessary displacement forward. By attention to this 
point, we materially reduce the initial hemorrhage, and avoid unnecessary 
stripping of the periosteum from the superior plate of the squama, a region 
not necessarily involved in the bone operation. Should it subsequently 
become necessary to do so, it will be found an easy matter to separate 
the muscle from its lower attachment and retract it upward. 

The hemorrhage following the initial incision is always more or less 
free, the chief bleeding points being (a) from the temporal muscle when 
it is cut, (b) from the sternomastoid fibres at the tip, and (c), between 








414 


TYMPANIC AND MASTOID OPERATIONS 


these points, from the divided periosteum rather than from the overlying 
tissues. When the initial bleeding is not excessive, the surgeon will save 
time by ignoring it until he has elevated the flaps anteriorly and pos¬ 
teriorly, when the chief bleeding points will be brought into better view, 
and many of the smaller ones will have ceased spontaneously. 

In deflecting the flaps, care should be taken to elevate the periosteum 
without unnecessary laceration or traumatism. This can be most easily 
accomplished by means of Langenbeck’s elevator (Fig. 212). With its 
bevelled edge placed firmly upon the bone and parallel with the edge of 
the incised periosteum, the latter can be elevated without laceration 
throughout the greater part of the incision. With practice this part of the 
operation can be done very quickly,— i.e., from a few moments to two or 
three minutes, according to the roughness of the cortex and the strength 
and thickness of the tendinous attachment. Naturally the most difficult 
part of the cortex to uncover is found just above the tip where we come 
upon the tough tendinous fibres of the sternomastoid muscle. These can 
in some cases be cleanly elevated from the bone by very careful use of the 
elevator, but in muscular subjects it is usually necessary to cut them away 
with the points of a pair of curved scissors. 

When the tip has been properly cleared, the anterior flap pushed for¬ 
ward so as to expose the suprameatal spine, and the posterior flap sepa¬ 
rated from the bone to a distance of about an inch, we have an exposure 
which in many cases is quite adequate to the requirements of the operation. 
There are cases, however, in which it is not. As soon, therefore, as it be¬ 
comes evident that the exposure of additional bone will facilitate the oper¬ 
ation, this can and should be obtained by the supplementary incision sug¬ 
gested by Whiting. Starting opposite the orifice of the bony meatus, this 
runs backward roughly at right angles to the initial incision (Fig. 223, c-d), 
thus dividing the crescentic posterior lip of the wound into two triangular 
flaps. These, properly deflected, usually provide easy access to all parts of 
the diseased mastoid (Fig. 224). 

The Bone Operation. —In attempting to present clearly the essential 
points of this important operation, I shall depend very largely upon a 
series of illustrations representing its successive steps. 

I. The initial opening into the mastoid is made by the removal of a 
strip of cortex whose posterior boundary is indicated by the heavy dotted 
lines in Fig. 224. It begins well forward,— i.e., from 4 to 5 mm. behind the 
suprameatal spine,—its anterior boundary closely following the posterior 
canal wall and anterior margin of the mastoid to the tip. For removing 
the cortex, the safest instrument is a gouge of medium size (Fig. 214). It 
should be held very obliquely, so as to remove a layer of bone not more 
than one-eighth of an inch in thickness. 

If we imagine a horizontal line tangent to the roof of the bony meatus 
and a vertical line tangent to its posterior wall, it is clear that these lines 
will cross each other just above and behind the spine of Henle (Fig. 224). 
Just behind their point of crossing is the point at which the gouge should 
enter the bone (x). It should be propelled by very moderate blows of the 


INITIAL REMOVAL OF BONE 


415 


mallet, and carefully guided along the anterior margin to the tip. Used 
in this way, even if the cortex be thin, and the sigmoid sinus situated far 
forward and near the surface, the latter is not likely to be injured, whereas, 
if the gouge be held more at right angles to the cortex and made to pene- 



Fig. 224.—Mastoid cortex adequately exposed for operation, x indicates point at which gouge 

should enter bone. 


4 

trate more deeply into the unexplored bone, there is distinct danger of 
opening the sinus, with resulting profuse hemorrhage and the grave pos¬ 
sibility of serious intrasinous infection. Ordinarily—i.e., when the mas¬ 
toid surface is free from unusual depressions—this anterior strip of bone 
may be removed with a single continuous excursion of the gouge. When 
the cortex is thin, the mastoid cavity is usually opened with the first layer 
of bone removed, but a thick cortex we may have to remove in successive 
lavers. The opening thus formed may then be widened by the removal of 
a second strip (Fig. 225). This enlarged opening discloses the diploic or 
pneumatic structures, according to the character of the bone. After t is 







































416 


TYMPANIC AND MASTOID OPERATIONS 


stage is reached, the writer usually makes no further use of the mallet or 
gouge, preferring to substitute other instruments which do their work 
without the jar, or concussion, incident to the use of the mallet. 

Note. —The advantage of the gouge over the chisel lies in the fact that the former 
simultaneously excavates and removes a shallow continuous layer of bone, whereas 
with the chisel one must outline the edges of small areas of bone which are then prised 
or lifted from their position. This is a slower process which is also attended with greater 
possibilities of injury to important structures below the cortex. 

II. The second step is the removal of the diploic or intercellular bone 
substance now exposed in the anterior part of the mastoid. This is most 
safely accomplished by means of a bone curette of medium size. In order 



Fig. 225.—Position of gouge in removing 
mastoid cortex. Dotted lines indicate posterior 
boundary of second strip of cortex removed. 



Fig. 226.—Representing the extent and outline 
of the initial opening usually made with the 
mallet and gouge. 


to avoid risk of injury to the sinus, the position of which we may not as 
yet know, the curette should at first be used with great care and with its 
cutting edge directed slightly forward toward the anterior plate of the mas¬ 
toid. In this way a deep groove is made, which hugs the anterior wall of 
the mastoid and is gradually deepened until the firm, harder bone repre¬ 
senting the floor of the general mastoid cavity is reached (Fig. 226). If 
the groove of the sigmoid sinus traverses this part of the mastoid, its 
arched bony plate will be detected by its harder, smoother surface; or it 
may be that the vessel itself may be exposed by the inadvertent removal 
at some point of its bony covering. This accident, while better avoided, 
need not cause anxiety beyond making us careful to avoid injuring its 
dural covering during the subsequent steps of the operation. 





































































TREATMENT OF MASTOID TIP 


417 



III. Further Removal of Cortex .—The next logical step is the removal of 
the remainder of the mastoid cortex. Having reached the stage shown in 
Fig. 226, we know that we shall have to further uncover the mastoid at 
least to the extent roughly shown by the dotted lines in Fig. 227. It is 
better to adopt a regular system in doing this,—starting either above and 
going downward toward the tip, or 

vice versa. Personally, I prefer to 
begin by removing the outer cortex 
of the tip, following this upward 
and backward, and finally remov¬ 
ing the outer w'all of the antrum. 

Undoubtedlv the best instrument 
for this work is a rongeur of appro¬ 
priate size and design. I prefer a 
rather large rongeur for working- 
backward toward the posterior mar¬ 
gin of the mastoid, and a smaller 
instrument for work about the tip 
and antrum. The advantages of the 
rongeur over the gouge or chisel are 
(1) absence of the jar or concussion 
which is inseparable from the use of 
mallet and chisel, a consideration of 
no little importance in some cases; 
and (2) the combined rapidity and 
safety with which it enables one to 

work. The one danger of the rongeur is the possibility of introducing the 
under blade too deeply or too far beneath an overhanging shelf of bone, 
and thereby including in its bite the membranous wall of the sinus. This, 
however, has never occurred in the writer’s experience, and with ordinary 
care can be easily avoided. 

IV. Treatment of the Tip .—With most American aurists it has become 
an axiom that in every case the tip should be removed. This dogma has 
long seemed to the writer to require some modification, or at least a clearer 
definition than is vouchsafed in most text-books. Does removing the tip 
mean that we shall in every case expose the posterior belly of the digastric 
muscle by removing the inner plate of the tip? Personally I do not be¬ 
lieve that it is always either necessary or advisable to do so. Unquestion¬ 
ably the tip cell or cells should be uncovered by removal of the external 
cortex, and the diploic or intercellular bone substance should be removed. 
If the inner plate thus exposed is diseased or so thin as to leave its nu¬ 
trition in doubt, it also should be removed. But if the exposed inner plate 
is composed of comparatively thick, healthy bone, I can see no valid 
reason for its removal, nor have I seen one advanced. On the contrary, by 
leaving it unmolested, we avoid useless injury of the digastric muscle and 
lessen the danger of secondary infection at this point. In such a case its 

27 


Fig. 227.—Illustrating the use of the rongeur in 
removing the mastoid cortex. 























418 


TYMPANIC AND MASTOID OPERATIONS 


lower margin should be rubbed smooth by means of a curette, but such 
part of the inner plate as is obviously sound and capable of maintaining 
its own nutrition should not be removed. 

V. Locating the Antrum .—Ordinarily there is no difficulty in locating 
the antrum. Situated at a variable depth from the surface, and at a point 
just above and behind the posterosuperior w r all of the bony meatus, it is 
found at the upper end of the original groove, or excavation (Fig. 226). 
Its identity may, if necessary, be confirmed by introducing a bent probe 
(Fig. 228), and passing its curved end forward through the so-called aditus 

ad antrum into the tympanic 
vault. If the end of the probe 
encounters no opening leading 
forward into the vault, we know 
that we have not entered the 
antrum. 

If the antrum is small, beginners 
occasionally have difficulty in reach¬ 
ing it because the excavation 
is either (a) not deep enough or 
(b) has not been extended suffi¬ 
ciently in a direction upward and 
forward. 

In bones of semisclerotic type 
the antrum is often exceedingly 
small, in some cases extending little 
if any beyond the limits of the 
space usually spoken of as the 
aditus. When in such a case the 
surgeon fails to locate the antrum 
in the situation in which he expects 
to find it, he may proceed to trace 
it in the following way: Pushing 
the anterior flap and auricle well 
forward, let him carefully note the 
position of the suprameatal spine 
and level of the posterior root of the zygoma (Fig. 229). Taking now two 
imaginary lines,— one horizontal and passing through the posterior root of 
the zygoma ( a-b ), and the other oblique and passing through the anterior 
and posterior ends of the suprameatal spine (c-d),—he has the angle, h-e-d. 
An arrow pointing forward and somewhat upward and bisecting this angle 
will necessarily point directly to the aditus, which may represent the only 
antrum present. As a supplementary guide, the surgeon may utilize the 
superior plate or roof of the mastoid process, following this forward to the 
antrum or aditus, of which its continuation forms the roof. 

When for any reason there is difficulty in locating the antrum, the use 



Fig. 228.—Diagram showing the use of the bent 
probe in locating the aditus. 























SURGICAL TREATMENT OF ADITUS AD ANTRUM 419 


of these lines not only provides the correct point of attack, but in the case 
of a low-lying tegmen antri insures against the possible error of entering 
the middle fossa, and perhaps perforating the dura and brain, under the 
impression that the curette has entered the antrum. 



VI. Surgical Relations of the Aditus .—It is often found, after the antrum 
has been cleared of pus and granulations, that the aditus is also filled with 
unhealthy granulations which it is our duty to remove. In using the curette 
for this purpose, the surgeon should bear in mind the relation of this space 
to the facial canal and horizontal semicircular canal (Fig. 230). 

Within the tympanum, or rather upon the inner tympanic wall, the 
prominence of the horizontal semicircular canal is seen immediately above 
the horizontal portions of the facial canal (see Fig. 15 on page 11). 
As they extend backward, however, the facial canal passes beneath the 
floor of the aditus and there bends downward, from which point it passes 
more or less vertically to its termination in the stylomastoid foramen. 
The semicircular canal, on the other hand, being in the horizontal plane 
and slightly above the facial canal, curves backward and lies behind the 
aditus (Fig. 230). In curetting the walls of the aditus, therefore, we must 
remember that beneath its floor is the bend of the facial nerve, while just 
behind its posterior wall is one aspect of the horizontal semicircular canal. 
From this the surgical deduction is clear that, while we may use the curette 
with freedom against the anterior wall and roof, it should be employed only 
with great care and gentleness against the posterior wall and floor. The 
surgeon should always direct the anaesthetist to watch the face closely for 
unilateral facial spasm while he is working within the aditus. 

Surgical Treatment of the Aditus .—Usually the tympanic lesion suffi¬ 
ciently antedates the mastoid symptoms to make this region a seat of 
advanced pathologic change. Frequently the mucosa is eroded and 
partly replaced by exuberant granulations. If these granulations are only 
partially removed from the aditus, what remains may shrink and the 





420 


TYMPANIC AND MASTOID OPERATIONS 


Horizontal 

semicircular 

canal 


Cross- 
section 
of facial 
canal at 
bend 


parts rapidly regain their normal character. On the other hand, a small 
amount of granulation tissue left in this situation may mark the site of a 
necrotic area in the underlying bone. Such a focus of disease, if not surgi¬ 
cally removed, may perpetuate .the 
tympanic lesion. There is no question - 
that many trying cases of delayed re¬ 
pair and some failures have.been due to 
this cause. 

Granulations attached to the roof 
and upper part of the posterior wall 
may be quickly and radically dealt 
with. Frequently a considerable mass 
of diploic tissue is attached to tegmen 
tympani, thorough removal of which 
provides a safer postoperative 
condition. 

Granulations occupying the floor 
of the aditus are frequently attached 
also to the short process and body of the 
incus, a fact which should be borne 
in mind since considerable care is nec¬ 
essary in some cases to avoid disloca¬ 
tion or even extraction of the incus. 
Particularly in operating on young 
Fig. 230.—Vertical section through the aditus. children is this danger a real one. Re¬ 
moval of granulations in this situation 
often brings the incus into view, and sometimes also the head of the malleus. 
In cases of long standing tympanic suppuration, which have not reached the 
stage characterized as chronic suppuration, exposure of one or both ossicles 
by careful removal of the outer wall of the vault may be necessary in order 
to bring the parts into a condition favorable to prompt tympanic repair. 
This, however, is exceptional. The contention of some surgeons that the 
incus should be exposed to view as a routine practice in all mastoid opera¬ 
tions does not appeal to me as well founded. 

VII. Outlining of Sigmoid Groove; Angle between It and Mastoid Roof .— 
In removing the diploic or pneumatic structures from the interior of the 
mastoid process, we reach in most directions the smooth bone of its limit¬ 
ing plates. Anteriorly we come upon the posterior canal wall and pre- 
mastoid plate; above, upon the inner plate of the tegmen antri; posteriorly 
and at a distance from an eighth of an inch (exceptional) to a half inch 
or more from the posterior canal wall, upon the firm arched plate of 
bone forming the osseous covering of the sigmoid sinus. Internal to and in 
front of the sinus groove is the plate separating the mastoid cavity from 
the posterior fossa of the skull and the cerebellum. The modern concep¬ 
tion of the requirements of the mastoid operation is that all these structures 








OBLITERATION OF ZYGOMATIC CELLS 


421 


should be outlined by the fairly complete removal of the intercellular bone 
substance. This is best done by means of a curette. For this purpose a 
large spoon curette is a safer instrument than a small one. Generally 
speaking, it is safer for the stroke, or sweep, of the curette to be up or 
down— i.e., from tip to roof or vice versa —rather than from before back¬ 
ward. When the sinus groove is encountered, its outline is traced by re¬ 
moving the diploic tissue from it and its immediate neighborhood. As the 
sinus groove is traced from below upward, it gradually, or in some cases 
rather suddenly, curves backward to join its parent, the lateral sinus. 
Between the upper surface of the bend of the sinus groove and the mastoid 
roof is found in some temporal bones a triangular space from which it is 
necessary to remove the diploic or cellular tissue. The rather thorough 
removal of the pneumatic or diploic structures throughout the mastoid is 
made necessary by the frequent finding of pus in cells deeply placed and 
at a distance from the main source of infection. 

VIII. Obliteration of the Zygomatic Cells .—Placed superficially— i.e., 
near the outer cortex—and corresponding roughly in position to the pos¬ 
terior root of the zygoma, is a collection of diploic or pneumatic spaces, 
popularly known as the zygomatic cells. They are to some extent present 
in practically all bones of diploic or pneumatic type. In very dense 
bones— i.e., those approaching the sclerotic type—they are frequently 
altogether absent. 

So far as I am aware, Whiting was the first to call attention to the 
importance of including these cells among those which should be removed 
in every case of suppurative mastoiditis operated upon. They may be 
exposed by continuing the removal of the outer cortex forward over the 
spine of Henle and along the posterior root of the zygoma, and extending 



Fig. 231.— Mastoid excavation completed, showing extensive development of zygomatic cells, 
usual removal of bono in this region is better indicated by Fig. 279. 


The 


this opening upward to the level of the inner plate which forms part of 
the floor of the mid-cranial fossa (Fig. 231). It is then an easy matter to 
obliterate and remove the cells thus exposed by means of a suitable curette. 




422 


TYMPANIC AND MASTOID OPERATIONS 


Whiting claims that lack of thoroughness in removing these cells has been 

the cause of many operative failures. 

Rational Thoroughness in Obliterating the Mastoid Cells. 
Whatever changes in our conception of the mastoid operation have occurred 
within the past decade have been in the direction of greater thoroughness. 
We now leave no considerable collection of cells unopened in any part of 
the mastoid. The cells of the tip, at the base of the zygoma, in the depth 
of the anterior portion of the mastoid, and in the angle between the bend 
of the sinus and mastoid roof, and sometimes behind the sinus groove, are 
removed to the extent of outlining clearly these various parts of the gen¬ 
eral mastoid cavity. To Whiting belongs the credit of having focussed 
the attention of aural surgeons on the importance of systematic, routine 
thoroughness in obtaining these mechanical results. While there is no 
doubt that these changes have been in the right direction, it is a question 
whether our zeal or enthusiasm has not led us into certain errors of over¬ 
statement, which in turn have led, in some cases, to somewhat exaggerated 
views as to the mechanical results for which we should strive. 

For example, if we say that every vestige of diploic or pneumatic cell 
structure should be carefully removed, we are advocating what in many 
bones is not only unnecessary but actually impossible. The accompany¬ 
ing figures (Nos. 232, 233, 234) were carefully drawn from a bone prepared 



Fig. 232. _Line of section extending through mastoid process and petrous portion of the temporal bone. 


by the writer. They show the presence of continuous chains of cells filling 
the mastoid, passing beneath the labyrinthine capsule and reaching to the 
apex of the petrous bone. The bone from which these illustrations were 
drawn is not unique. Even better than the pictures, a study of the bone 
itself impresses one with the futility of attempting to follow up and remove 









RATIONAL THOROUGHNESS IN MASTOID SURGERY 423 


literally all the cellular structures to which the mastoid operation may 
provide access. 

There is one other point in regard to which the author wishes to record 
the results of his personal observations. A distinguished surgeon, in de¬ 
scribing the technic of the mastoid operation, says, “The concluding step 



Fig. 233. —Pneumatic spaces extending from mastoid process to apex of petrous bone. 



Fig. 234.—Continuous chains of pneumatic spaces extending from mastoid to petrous 

portion of the bone., 


in the removal of bone now consists in smoothing off the rough diploic 
structure which invests the sigmoid groove until the inner plate of the skull 
presents a glistening, even surface, which sort of a polish a large dull curette 
moved gently and rapidly over it will speedily enforce.” My own observa¬ 
tion and experience have led me to believe that the above represents a 
super-refinement of technic which serves no particularly useful purpose 
and which may reduce to a dangerous degree the vitality of the bone. I 
have seen skilful operators so polish their bone surfaces as to create a bone 
cavity of striking smoothness, and in the same cases I have seen granula¬ 
tions form and local recovery occur only after a period of unusual delay. 
In my own operative experience I have repeatedly observed that when in 
the interest of thoroughness I have obtained a particularly smooth and 






424 


TYMPANIC AND MASTOID OPERATIONS 


even surface, repair, as represented by the formation of a covering of 
healthy granulations, has been proportionately slow. 

As aural surgeon to the Willard Parker Hospital for Infectious Dis¬ 
eases, I have during the past eight years had a fairly large experience in 
operating upon children suffering from infectious diseases. In these cases, 
it is certainly a fact that if we attempt by curettage to obtain smooth, 
even surfaces, we shall have failure of local nutrition and necrosis, calling 
for secondary operation, in an exceedingly large percentage of cases. 

The point I wish to emphasize is that after we have eliminated all 
masses of cellular or diploic tissue which might be suspected of harboring 
concealed pus or foci of infection, and have thereby defined the limiting 
walls of the mastoid cavity, we have fulfilled the purpose of the operation. 
To go further and curette these walls into surfaces of even and polished 
smoothness may reduce their vitality to a point seriously interfering with 
normal repair. 

Before taking up the post-operative treatment, a word should be said 
of certain operative incidents which occasionally occur, either by accident 
or intention, during the course of a mastoid operation. 

Exposure of Dura .—It is not uncommon, either as a result of necrosis, 
accident, or the intentional removal of diseased bone, that the dura in 
contact with the cerebral surface of the tegmen antri is exposed. Unless 
the dura itself is punctured or torn, this occurrence need cause the sur¬ 
geon no anxiety. An area of exposed dura presenting in the mastoid 
wound is certainly a safer condition than dura covered by doubtful or 
diseased bone. From the edges of the opening in the cranial plate any 
rough or sharp surfaces or points should be removed. The dura exposed 
through such an opening, if not itself lacerated, will usually be covered by 
healthy protective granulations even sooner than the adjacent bone 
surfaces. 

Exposure of Sigmoid Sinus .—Accidental or intentional exposure of 
the sigmoid sinus, if its dural covering is not injured, usually leads to no 
untoward consequences. When a very small surface of the sinus has been 
accidentally exposed, it is safer, in the writer’s opinion, to enlarge the 
opening to the extent necessary to expose an area at least three-eighths of 
an inch wide by a half inch long. This enables the surgeon to determine 
definitely that no traumatism of the dura has occurred, and in case of 
subsequent sinus trouble provides an opening which may be quickly 
enlarged to the extent required for further surgical intervention. 

The surgical technic of exposing the sinus will be given in connection 
with the surgical treatment of infective sinus thrombosis. 

Accidental Opening of the Sinus .—An experience which probably comes 
to every aural surgeon is that of accidentally nicking or tearing the sinus. 
The immediate result is naturally a very copious hemorrhage. Blood 
pours into the wound in a volume naturally disconcerting to the inex¬ 
perienced surgeon. When the bone covering the sinus is diseased and 
adhesions between the sinus and inner bone surface have occurred, injury 
or tearing of the sinus wall may be difficult to avoid. It is a wise precau- 


POSTOPERATIVE TREATMENT 


425 


tion, therefore, to have in readiness a supply of small, tightlv-wound rolls 
of sterile iodoform gauze, of the thickness find length shown in Fig. 235. 
One of these, taken up on the points of an ordinary thumb forceps, is 
usually easily applied over the bleeding point and will control the hemor¬ 
rhage. If the hemorrhage is not 
controlled by one roll, another 
placed alongside of it usually will. 

The gauze roll is held by an assist¬ 
ant upon the opening in the sinus, 
but on no account should be forced 
into it, nor is it usually necessary 
to compress the vessel so as to 
obliterate its lumen or reduce its 
calibre. Bleeding having been 
controlled, the assistant holds the gauze roll in position, while the surgeon 
proceeds calmly and systematically with his operation. 

The Element of Time in MAstoid ►surgery. In operating upon 
the mastoid the primary aim of a good surgeon is not speed, but the safety 
of the patient and completion of an adequate and perfect operation. On 
the other hand, prolonged anaesthesia is not without risks, and any unnec¬ 
essary delay is an element of danger. Ordinarily a simple mastoid opera¬ 
tion should be completed in a half to three-quarters of an hour, and only 
in a case of exceptional difficulty should it exceed an hour. The skilful 
surgeon works without apparent haste, but attains his result quickly 
because each thing he does accomplishes some essential step in the op- 

This deliberate but effective time-saving can be attained only by the 
adoption and rigid following of some systematic plan of attack plus the 
development of a certain degree of operative skill. If the surgeon begins 
to remove the tip, leaves it to define the sinus groove, and before this is 
completed is diverted to an attack upon the zygomatic cells, in short, it 
he proceeds with his work without system and in haphazard order, he 
mav eventually complete a creditable operation; but progress is likely to 
be "slow, and the chances that some essential step will be overlooked are 
increased. In describing the bone operation, I have therefore taken up 
separately the successive steps in the order which should be observed by 

the surgeon. . 

Postoperative Treatment. —Whatever changes have occurred m 

recent years in the theory and practice of mastoid surgery have related to the 
treatment of the soft parts rather than to the bone operation. The gauze- 
packed open wound has given place to the partially closed wound T is 
transition, though gradual and in no way spectacular, is of greater im¬ 
portance than is generally realized. To the patient it means a quicker 
average recovery, infinitely less suffering and a better average cosmetic 
result. It may be worth while, therefore, briefly to compare the two 

Open Wound Method.— By the older method, the wound cavity on com- 



Fig. 235. —Iodoform gauze plugs for control of 
hemorrhage in case of accidental opening of sinus. 


































426 


TYMPANIC AND MASTOID OPERATIONS 


pletion of the operation was firmly packed with plain or iodoform gauze. 
The gauze was used in sufficient quantity to project somewhat above the 
level of the bone cavity, the flaps being thus held apart. Subsequent dress¬ 
ing: while the outer dressing was commonly changed within twenty-four 
hours, the wound packing was usually allowed to remain until the fourth 
or fifth day after the operation. When first removed it was not uncommon 
to find a clean wound-surface of practically bare bone. This was considered 
a perfectly satisfactory condition. Subsequently the dressings were changed 
on alternate days, the successive dressings differing from the first only in 
the fact that rather less pressure was used. 

Generally speaking, the ultimate results from this treatment were fairly 
good. As offsetting this fact, must be mentioned certain recurring mis¬ 
haps which seem to have been more or less directly attributable to the 
method employed: 

(1) In a fairly large percentage of cases ending in recovery, healing 
was unduly delayed, a lapse of 10 to 12 weeks between operation and final 
healing being by no means uncommon. 

(2) In a proportion of cases certainly larger than are met with to-day, 
secondary operations for removal of diseased bone were necessary. 

(3) In a considerable percentage of cases, healing, usually considerably 
delayed, occurred with the formation of a permanent and unsightly de¬ 
pression behind the ear. This unfortunate deformity is comparatively 
rare to-day. 

We would now regard all or any of these mishaps as logical results of the 
post-operative technic; for it is clear that the continued gauze packing 
might (a) inhibit the formation of the healthy granulations and thus pre¬ 
vent or retard recovery; (b) interfere with the local blood supply, with con¬ 
sequent loss of vitality and osseous necrosis at certain points; and finally 
(c) by inhibition of normal tissue repair, prepare the way for the inevitable 
growth of integument from the flap margins into the wound cavity, this 
giving rise to a disfiguring depression behind the ear. 

The general tendency during the past decade has been away from the 
old plan of wide open gauze-packed wounds and toward more or less closed 
wounds protected by some form of drainage. Under favorable surgical 
conditions,— i.e., in the case of wounds lined with apparently healthy 
bone or in which comparatively small areas of healthy dura have been ex¬ 
posed,—the method employed by most progressive surgeons to-day is about 
as follows: the wound cavity is flushed with normal salt solution and care¬ 
fully inspected to see that no bone particles are allowed to remain. A wick 
of plain sterile gauze, so infolded that no threads may be left when it is 
withdrawn, is placed in the depths of the wound with one end at the aditus, 
the other emerging at the lower end of the wound. Over this the flaps are 
approximated and united throughout from the upper extremity of the 
wound to within half an inch of its lower, or tip, end. This may be done by 
metal clips or, as the writer prefers, by interrupted silk-worm gut sutures. 
The sutures are carried preferably through the entire thickness of each flap 


POSTOPERATIVE TREATMENT 


427 



Fig. 236. Operation of mastoidectomy 
completed. 


so as to approximate and unite not only the skin, but also the periosteal, 
edges. Such a wound presents somewhat the appearance presented by 
Fig. 236. A gauze wick fills the audi¬ 
tory canal, the whole being protected by 
the usual large dressing of sterile gauze. 

The bandage used by the writer is com¬ 
fortable, does not slip, and has the 
appearance shown in Fig. 237 

The dressings are changed daily. On 
the day following the operation the wick 
is withdrawn, and a pad or ball of 
sterile cotton is pressed gently against 
the lower wound-opening to take up by 
capillary traction any surplus serum or 
secretion. The wick removed is then re¬ 
placed by a smaller one which is intro¬ 
duced only from three-fourths of an inch 
to an inch into the wound. Thereafter 
the wicks are changed at each daily 
dressing until there is evidence that they 
are no longer needed. 

Dependence on the foregoing treatment is based on the hypothesis that 
the first wick used establishes a drain or pathway of least resistance along 

which pus or serum escapes as long as 
drainage is necessary. The smaller 
wicks used in subsequent dressings 
merely maintain the opening at the 
lower end of the suture line. 

There are two fairly reliable signs 
that this treatment is progressing 
favorably, namely, (1) progressive 
and fairly rapid return of drum 
membrane and tympanic landmarks 
to a normal appearance; and (2) pro¬ 
gressive diminution of discharge from 
the opening in the post-auricular 
wound. 

I would abandon this treatment 
and open the wound in any case in 
which the tympanic structures did 
not within a reasonable time show 
progressive improvement. On the 
other hand, I might persist during a 
considerable period in spite of a fairly 
profuse, if diminishing, post-auricu¬ 
lar discharge. 



Fio. 237.—Mastoid bandage. 











428 


TYMPANIC AND MASTOID OPERATIONS 


Interpretation of Pus. —It is almost a habit of mind to think of pus as a 
danger symptom since it always indicates a focus of infection, present or pre¬ 
existing. In reality, pus per se represents danger only if confined or if its secre¬ 
tion, or production, is more rapid than its elimination. A raw or granulating 
wound without secretion is, of course, a surgical impossibility. Given, there¬ 
fore, a partially closed wound from which we believe that we have eliminated 
the primary focus of infection, we need not be too ready to take alarm at 
a discharge which may represent only a stage in the process of repair. 

I have known wounds treated by this method to have every appearance 
of being practically healed within ten days. More wounds are healed within 
three to five weeks. Some, for one reason or another, do not progress 
satisfactorily, but after separation of the flaps, there follows a more rapid 
process of healing than by the older method. 

Theoretically this plan of treatment seems to meet the following re¬ 
quirements: (a) it provides reasonable and adequate drainage; (b) it 
utilizes every normal structure, bone and soft parts in the process of repair; 
(c) it secures the maximum vascular supply to the parts; and, perhaps 
most important of all, (d) it subjects the wound in process of repair to the 
least possible mechanical disturbance. 

Contraindications. —That there are contraindications to this method goes 
without saying. As such I would consider surgical injuries to the sigmoid 
sinus, physical signs of disease in an exposed sinus wall, and unusual ex¬ 
tension of bone necrosis. 

Pronounced constitutional symptoms of septic absorption would also 
call for an open wound, since in such cases the systemic disorder, and not 
the local lesion, would be the first consideration. 

In uncomplicated cases of suppurative mastoiditis the postoperative 
symptoms are usually not pronounced. During the first twenty-four hours, 

-—sometimes prolonged to forty-eight hours—there may be moderate eleva¬ 
tion of temperature, the so-called “ postoperative temperature. ” In my ex¬ 
perience, this is the exception rather than the rule. High temperature, and 
particularly continued high temperature, may indicate retention of secretion 
or pus, and would call for opening, and inspection of the depths, of the wound. 
After cleansing the wound of retained pus or infected clot, or correcting 
whatever condition may be at fault, the lips of the wound may be allowed 
to fall together, drainage being provided for as before by a small wick. 

What has been said above refers to the general run of cases. Obviously, 
there are certain cases in which by reason of one or other of several con¬ 
ditions— e.g., surgical accidents to dura or sinus wall, superficial changes 
in exposed dura, unusually wide-spread bone disease, etc.—safety may call 
for an open wound. In such cases, we now use light packing with sterile 
gauze until the bone cavity is lined throughout with healthy granulations, 
when the question of hastening recovery by a plastic closure operation may 
be taken into consideration. 

Exuberant Granulations Springing from Carious Bone. —If areas of dis¬ 
eased bone are overlooked at the time of the operation, or if the vitality of 


POSTOPERATIVE TREATMENT 


429 


the bone is in certain regions destroyed, healing will not take place, and the 
need of opening the wound will soon be in evidence. The diseased 
areas are likely to be differentiated from surrounding healthy struct¬ 
ures by one or other of two conditions, i.e., either (a) the diseased bone 
is rough, bare and often devitalized in appearance; or (b) is covered with 
exuberant, flabby granulations. These granulations offer no resistance to 
the probe, which finds its way easily to the underlying rough surface 
which is characteristic of carious bone. When the diseased area is cir¬ 
cumscribed and small, it may be possible under cocaine to remove with a 
curette the necrotic bone, after which rapid healing may take place. When, 
however, one has reason to believe that postoperative failure to heal is due 
to an extending area of necrosis, the shortest and safest road to recovery 
is usually by way of a secondary operation under full anaesthesia. 

Arrested Repair .—A postoperative condition, of which I have seen no 
mention-in text-books, but with which the surgeon has occasionally to deal, 
is characterized by the abortive type of granulations which line the bone 
cavity. Postoperative repair seems at first to follow a perfectly normal and 
favorable course. The bone cavity is soon lined by a layer of firm and 
apparently healthy granulations. The tympanic condition shows progres¬ 
sive improvement, and within a reasonably short period the drum mem¬ 
brane heals. In the postauricular wound, however, the process of repair is 
arrested. There is little or no pus, and in fact not more secretion than is 
inseparable from a granulating wound. The granulations themselves, though 
of healthy appearance, are stationary,— i.e., the process of tissue-building 
seems arrested. Do what we may to increase the local blood supply and 
thereby stimulate a normal growth of new tissue, the aditus remains open, 
and the postauricular wound persists as a cavity of very considerable size. 
In my experience this condition— i.e., arrested repair without evidences of 
osseous necrosis—is almost invariably an expression of anaemia or of 
some otherwise lowered constitutional state. 

The treatment offers an alternative between two methods,—viz., (a) we 
may allow the skin from the edges of the wound to extend into, and line, 
the wound cavity, in which case we must prepare the patient for a perma¬ 
nently disfiguring depression behind the ear; or (b) we may close the 
wound by a plastic operation. In the writer’s experience the latter has 
been a uniformly successful procedure. The operation requires complete 
anaesthesia and preparation of the operative field as for the original opera¬ 
tion. The soft parts are elevated from the bone for a distance of an inch 
and a half, or more, from the posterior border of the wound. This results 
in a sort of pocket between the bone and its periosteal covering. The 
anterior flap, which has usually become strongly adherent to the subjacent 
bone, is lifted from its attachments. The object of these manoeuvres is to 
release both the anterior and posterior flaps of the wound, so that they 
may be brought together without tension and sutured. If this requires 
forcible traction, the periosteum must be elevated from the bone to a 
greater distance behind the ear. This elevation of the posterior flap must 
28 


430 


TYMPANIC AND MASTOID OPERATIONS 


be extended until the edges of the wound can be brought together abso¬ 
lutely without tension. Unless this is done, the sutures will not hold,— 
i.e., they will “slough out.” Usually the skin has to some extent become 
infolded over the edges of the wound, and must be dissected up, or cut 
away, in order to bring raw surfaces together. The granulations within 
the mastoid wound are now removed with a curette and the cavity allowed 
to fill with blood. The prepared lips of the wound are now brought to¬ 
gether and united by interrupted silkworm-gut sutures, except at the lower 
end of the wound. Here a minute gauze drain is introduced to a distance of 
not more than a half inch. A large protective dressing of sterile gauze is 
then applied. From the day of the operation, the dressings should be 
changed daily. On the day after the operation, removal of the wick from 
the lower end of the wound is followed by the escape of a considerable 
quantity of serum. Very gentle pressure over the suture line serves to 
further rid the wound of serum seeking escape. A wick similar to the one 
removed is then introduced. This is removed on the following day, after 
which, as a rule, no wick should be introduced. The sutures are usually 
removed on the fifth or sixth day, and a day or two later all dressings are 
discontinued. 

In my experience, this procedure has been invariably successful in 
prcperly selected cases,—one indication of its suitability being a drum 
membrane and tympanum which have practically regained their normal 
condition. 

As particularly typical examples of this class, I may cite two of my own 
cases,—one that of a chlorotic school-girl of sixteen, the other an old 
gentleman of sixty-seven years. Neither of these patients would have 
looked amiably upon the suggestion of a large permanent depression be¬ 
hind the ear. In both the blood examination showed a markedly reduced 
percentage of haemoglobin. In each case the plastic operation was un¬ 
dertaken only after months of effort to stimulate sluggish, but otherwise 
healthy, granulations to more vigorous growth. The operation in each 
case was followed by healing within a week, without any disfiguring depres¬ 
sion. Recovery has been permanent in each case. 

Before leaving the subject of the mastoid operation, I wish to say a 
word as to the treatment of the tympanum both at the time of, and fol¬ 
lowing, the operation. If the opening in the drum-head is not sufficient 
to provide free drainage, it is safer to reincise it at the time of the 
operation. At each change of dressings, the ear should be thoroughly 
cleansed of pus, and dried, and the canal packed with sterile gauze. 
Rapid improvement in the condition of the middle ear, with early heal¬ 
ing of the drum membrane, usually foretells a fairly rapid healing of the 
mastoid wound. Lack of care in keeping the canal free of pus is probably 
a cause of failure, and certainly of delayed healing, in a certain percentage 
of cases. 

The “Blood-clot Operation” (Blake, Reik). —The use of the 
blood-clot to promote early filling of the so-called dead space of the mastoid 


THE “ BLOOD-CLOT OPERATION ” 


431 


wound, and incidentally to obtain primary healing of the outer wound, has 
added an interesting and instructive chapter to our knowledge of mastoid 
surgery. Since the bone operation does not differ from that in which the 
open method of after-treatment is used, the whole procedure may be 
described rather briefly. 

The preparation of the patient— i.e., operative field—is exactly as 
described for the older method. The drum membrane, even though show¬ 
ing a fairly large perforation, is reincised in order to provide the freest 
possible drainage from the tympanum. The postauricular incision through 
the soft parts differs from that used in the regular operation in being 
placed a little further behind the postauricular attachment,— i.e., it com¬ 
mences at or below the tip and is carried upward following a curvilinear 
direction parallel with, but a half inch behind, the attachment of the auricle. 
Especial care should be taken not to injure the periosteum. Unless abso¬ 
lutely called for, the supplementary horizontal incision should be omitted, 
and, as the primary incision is a quarter of an inch further back, i.e., 
from the auricular attachment,—this additional space is available for the 
bone operation. 

When the bone operation is completed, the cavity is washed out with 
normal salt solution, dried, and then allowed to fill with blood. 1 he an¬ 
terior and posterior flaps (soft parts) are then brought together, the edges 
carefully approximated, and held by interrupted sutures of silkworm gut. 
In this way the wound is entirely closed except at the lower end, which is 
left open. “The lower portion should be left free for serous outflow, and 
this outflow should be assured at each subsequent dressing'’ (Blake). 
Over this a large protective dressing of sterile gauze is applied. 

The postoperative treatment consists chiefly of daily changes of the 
protective dressing, strict care being observed to do nothing which might 
carry infection into the wound. The stitches are removed in from five 
to seven days. In favorable cases the wound, so far as further caie is 
required, may have every appearance of being quite healed in less than two 
weeks from the time of operation. 

The facts which its advocates urge in favor of the adoption of this 

operation may be stated as follows: 

1. The blood-clot itself has been proved to possess a decided bactericidal 
property; and this is depended upon to counteract any germs left in the 

mastoid wound, and to prevent reinfection. 

2. In surgical diseases and injuries of the long bones the use of the 
blood-clot has provided a reticulum or scaffolding upon which the new 
tissues have seized,—the clot becoming quickly organized and finally 
converted into permanent osseous tissue. The cavity resulting from the 
mastoid operation is regarded as providing a favorable field for this con¬ 
servative process. 

3. In actual experience a large proportion of the cases operated upon 

by this method are said to have been successful. 

4. When the blood-clot method is successful, the patient is saved much 


432 


TYMPANIC AND MASTOID OPERATIONS 


postoperative pain and discomfort, and, in the case of wage-earners, the 
loss of time from work is only a small fraction of the postoperative period 


bv the open method. . ... , ,. 

As to the danger of the closed wound m cases in which postoperative 

infection occurs, Reik holds that a remaining focus of infection wiU involve 

the clot itself sooner than normal living tissues, and that the natural 

tendency, when a sufficient amount of septic material has been left in the 

wound to interfere with natural healing, is toward destruction of the clot 

and consequent breaking down of the wound margins; hence the dangers to 


life are purely hypothetical.” . . t(rr . 

As to the cases in which the clot becomes infected, Blake says, I e 

persistence of the blood-clot during the period of its protective viability 
only, even though it then breaks down and comes away entirely, results in 
the formation of foundation granulomata, which are a basis for subsequent 
repair, with speedier and more satisfactory results in healing than are 
obtainable when the wound is dry-packed from the beginning. 

In the writer’s view, the chief objection to the adoption of the blood- 
clot method is that in cases of severe tympanic infection we are obliged to 
assume a postoperative escape of pus from the vault backward through 
the aditus into the space formerly constituting the antrum. Even if this 
does not result in postoperative reinfection of the entire wound, we are 
deprived of the use of the aditus as a means of draining the vault. In 
operating by the open method I believe that the usually rapid healing of 
the tympanic lesion is due very largely to postoperative drainage through 
the aditus. The blood-clot operation sacrifices this advantage. I should, 
therefore, expect tympanic resolution to be slower and less certain when 
the wound is closed at the time of operation than when the open method 
is employed. Those interested in the blood-clot operation are referred 
to the papers mentioned below. 4 


SURGICAL TREATMENT OF CHRONIC MIDDLE-EAR SUPPURATION. 

Radical Mastoid Operation; Schwartze=Stacke Operation. — Defi¬ 
nition: To otologists everywhere the term “radical operation ” signifies 
an operation which aims to relieve chronic middle-ear suppuration by the 
conversion of the middle ear, antrum, and any diseased spaces within the 
mastoid into a single cavity, which is primarily drained through the ex¬ 
ternal auditory meatus, and ultimately lined by integument continuous 
with that of the membranous canal. With complete epidermization, all 
mucopurulent discharge ceases. 

4 Blake, C. J.: The Value of the Blood-clot as a Primary Dressing in Mastoid Oper¬ 
ations, read at the Toronto meeting of the British Medical Association, 1906. 

Reik, H. O.: The Blood-clot Dressing in Mastoidectomy, Considered Physiologi¬ 
cally, Jour. American Medical Association, March 31, 1906. 

Reik, H. O.: Some Facts and Figures relating to the Blood-clot Dressing in Bone 
Surgery, Trans. American Otological Society, 1906. 

Sprague, F. B.: The Blood-clot Mfcthod of Wound Repair in Aural Surgery, The 
Laryngoscope, St. Louis, September, 1906. 






THE RADICAL OPERATION 


433 


The indications for the radical operation have already been stated 
(pages 216 to 217) and need not be repeated here. The writer wishes, how¬ 
ever, to reiterate the great importance not only of making a thorough 
physical examination of the ear, but also of testing carefully the patient’s 
hearing power, and also the functional soundness of the static or vestibular 
apparatus. The demonstration of fairly acute hearing power should 
certainly be weighed carefully in considering the advisability of an opera¬ 
tion which sometimes influences the hearing unfavorably; and the evidence 
of a diffuse suppurative lesion of the labyrinth, even though all active 
symptoms may have long since subsided, is recognized as a contra-indica¬ 
tion to the radical operation, unless we are justified in operating at the 
same time upon the infected labyrinth. 

Preparation of the Patient. —The method of preparing the operative 
field has already been described. After the side of the head has been 
shaved, the auditory canal should be wiped out, then filled with peroxide of 
hydrogen, and finally irrigated with a 1 in 2000 solution of bichloride of 
mercury. It is then packed rather firmly with a strip of plain sterile 
gauze. The cleansing and sterilization of the auricle and the shaved area 
behind it are carried out by exactly the same method as for the simpler 
mastoid operation. 

The incision begins below at the tip and follows a curvilinear direc¬ 
tion behind the ear to a point above the upper attachment of the auricle, 
its centre being five-eighths of an 
inch behind the postauricular attach¬ 
ment (Fig. 238). From the tip to 
the temporal ridge this incision 
should divide all tissues down to the 
bone, while above the temporal ridge 
it may reach only the temporal 
fascia,— i.e., it is not necessary that 
it should include the temporal mus¬ 
cle. In elevating the anterior flap 
thus formed, great care should be 
taken not to tear or mutilate the 
periosteum which, it must be re¬ 
membered, is destined to form the 
outer wall of the cavity proposed by 
the operation. Richards has called 
attention to the following advan¬ 
tages of a very wide anterior flap,— 
viz., (a) when the posterior wound 
is closed, the suture line will lie be¬ 
hind the posterior margin of the excavation and have, therefore, the firm 
support of the mastoid cortex; (b) the outer wall of the bone cavity will 
be formed by an unbroken surface of periosteum, whereas, with a primary 
incision close to the auricular attachment, the suture line would form part 
28 



Fig. 238.—Postauricular incision for the radical 
operation. 





434 


TYMPANIC AND MASTOID OPEEATIONS 


of the outer wall of the bone cavity and granulations forming there might 
project into it and interfere materially with final healing. 

The anterior flap is elevated and pushed forward so as to expose a 
large part of the outer rim of the bony meatus,— i.e ., posterior, superior, 
and inferior aspects. The membrano-cartilaginous meatus is at the same 
time completely separated from the posterior wall of the bony meatus 
by means of a narrow, curved periosteal elevator. The suggestion of 
Stacke, that the inner end of the membranous canal wall— i.e., near the 
attachment of the drum membrane—be cut through with an angular 
knife, is quite unnecessary, since the membranous canal tears away 
easily at this point and with less traumatism than would be caused 
by the knife. 

When the radical operation is not successful, its failure is usually a 
result either of postoperative neglect or of the surgeon’s neglect or omis¬ 
sion of some apparently minor technical point during the operation. In 
describing these essential details, we shall take up separately the successive 
steps of the operation in the order in which they occur in the actual 
operation. 

I. Removal of the Outer Wall of the Antrum (Fig. 239).—Generally 
speaking, it is safer—and certainly for the beginner—to open the antrum 
before attempting to remove the posterior wall of the bony meatus. For 
this purpose, the gouge (Fig. 214) is the safest as well as the most con¬ 
venient instrument. The initial removal of cortex is indicated by the 
excavation in Fig. 239. The gouge is made to enter the bone just above 
and behind the suprameatal spine, and, being carefully guided along the 



Figs. 239 and 240. —First 



stages of radical operation. 


anterior border of the mastoid, removes a layer of bone not more than an 
eighth of an inch in thickness. Usually in cases of long-standing middle- 
ear suppuration, the cortex is very thick, and it is necessary to remove 
several layers of bone before the interior of the mastoid is reached. By 
hugging the posterior canal wall, and very gradually deepening the narrow 




















THE RADICAL OPERATION 


435 


excavation thus outlined, we minimize the danger of injury to the sig¬ 
moid sinus. If, in removing the cortex, part of the outer margin of the 
posterior canal wall is shaved off, this does no harm, and simply antici¬ 
pates the next step of the operation. As soon as the exposure of diploic 
tissue or pneumatic spaces shows that we have entered the mastoid, we 
should deepen this space by means of a curette, keeping its 
cutting edge at first directed somewhat forward and curet¬ 
ting in the direction of the posterior canal wall rather than 
backward. Using the instruments in this way, we are not 
likely to injure the sigmoid sinus, even should its course lie 
far forward in the anterior half of the mastoid. When we 
have removed the cellular tissue corresponding to the first 
opening in the cortex, it is well to explore the boundaries of 
this excavation by means of a silver probe, the end of which 
has been bent almost at right angles with the shaft. By this 
means we may obtain the following data,—viz.: (a) If its 
bent extremity finds a passage or opening leading from the 
upper end of the excavation forward into the tympanic 
vault, we know that we have entered the antrum; (b) by 
passing it directly upward, we ascertain the height or level 
of the tegmen antri; and (c) by passing it backward beneath 
the cortex, should a space here exist, we may determine the 
extent of overhanging cortex to be removed in this direction. 

It may be that this use of the probe will show the excava¬ 
tion to extend beneath the cortex to the extent shown by 
the dotted lines in Fig. 239. The cortex must then be re¬ 
moved up to the limits ,so outlined. This additional removal 
of bone completes the first stage of the operation, and leaves 
a bone excavation somewhat resembling that shown by 
Fig. 240. 

II. Removal of the Posterior Canal Wall .-—The outer two- 
thirds of the posterior canal wall, having no important sur¬ 
gical relations, may be removed rather rapidly. At the 
start, we may save time and prepare the way for the chisel 
by biting out a wedge-shaped segment with a rongeur. In 
using the rongeur we should remove the bone as nearly as 
possible along its attachment to the roof. After removing 
the outer half in this way, the chisel is by far the safer in¬ 
strument. The remaining portion is now dealt with in the 
following way: With a Jansen chisel (Fig. 241), the rough 
upper margin left by the rongeur is chiselled away from the 
roof in thin vertical layers to the depth removed by the ron¬ 
geur. The chisel is now used to lower the canal wall from without in¬ 
ward,—beginning below and cutting in thin layers upward and inward 
toward the roof. By using the chisel alternately along its outer margin 
and along the line of its attachment to the roof, the posterosuperior canal 


Fig. 241. 
—Jansen’s 
chisel. 



































436 


TYMPANIC AND MASTOID OPERATIONS 


wall is soon reduced to the narrow inner rim, or bridge, shown in Fig. 
242. By this use of the chisel,— i.e., along its attachment to the roof,— 
the thinnest portion of the resulting inner margin, or “bridge” (a), is 

placed high in the tympanum,— i.e., 
above the level of the horizontal por¬ 
tion of the facial canal. Up to this 
stage of the operation the lower half 
of the posterior canal wall ( b ) has 
been lowered only in moderate degree, 
and certainly not sufficiently to en¬ 
danger the descending portion of the 
facial canal which lies beneath. 

The removal of the remaining rim 
of the posterosuperior canal wall pre¬ 
sents some difficulty to the beginner 
on account of the danger of injury to 
the bend of the facial canal and hori¬ 
zontal semicircular canal which lie 
beneath. While the experienced aural 
surgeon has little difficulty in dividing 
the bridge with a chisel held firmly 
against its highest point, it is an instrument which must be handled with 
care. Korner uses a slender-bladed rongeur which removes the upper end 
of the bridge by a single bite. Richards believes that a small curette, 
introduced beneath the bridge from behind and pressed firmly against its 
upper attachment, is the safest instrument for this stage of the operation. 
It is a safe method only when the inner segment has been previously 
reduced to an extremely thin rim of bone. The writer some years ago 
invented a special forceps (Fig. 250), in connection with which he described 
a method of removing the posterior canal wall which eliminates completely 
the danger of injury to the facial nerve or horizontal semicircular canal. 
This method will be referred to later in connection with anatomical con¬ 
ditions for which it may be of special value. With a larger experience, 
the writer is inclined to believe that with the average run of temporal bones 
the work can be done quite safely by the careful use of either rongeur, 
chisel, or curette, according to the skill of the individual in the use of one 
or other of these instruments. 

The method usually employed by the writer is as follows: The re¬ 
maining inner margin of the posterosuperior canal wall having been 
reduced to a delicate bridge of bone having only a slender attachment 
above to the roof, a small straight-edged chisel is applied at this point 
—i.e., hugging the roof—and the bone divided by a very slight tap of the 
mallet. The slightest tap is all that is required, the horizontal semi¬ 
circular canal being endangered by a too vigorous blow. The bone 
having been thus divided above, a small curette is introduced from behind 
beneath the bridge, which is then lifted from its lower attachment, should 



Fig. 242. — Radical operation; a, shallow 
“bridge” formed by inner margin of postero¬ 
superior canal wall; b, remaining lower half 
of posterior canal wall. 










THE RADICAL OPERATION 


437 



Fig. 243.— Radical operation, after removal 
of “bridge" formed by posterosuperior canal 
wall; a, roof of bony meatus; b, facial spur, 
formed by remaining lower half of posterior 
canal wall; c, dotted line indicating course 
of facial canal. 


this not have been completely fractured. Removal of the bridge com¬ 
pletes the second stage of the operation, and leaves a cavity similar to 
that shown by Fig. 243. 

III. Removal of the Roof of the Meatus. —The posterosuperior canal 
wall having been removed, we should turn our attention to the plate of 
bone forming the roof of the meatus 
(Fig. 243). This should be so thor¬ 
oughly removed as to bring the roof 
of the vault and the superior wall of 
the bony meatus into a continuously 
even or unbroken surface. This may 
be done with a sharp bone curette,— 
either the Richards instrument or the 
ordinary sharp spoon curette,—which 
removes the bone quickly from within 
outward. This part of the operation 
is of considerable importance, since a 
ridge of bone separating the roof of 
the attic from that of the bony canal 
provides an unfavorable surface for 
epidermization, and leaves an angular 
space at the junction of the roof and 
outer wall of the vault in which per¬ 
sistent granulations are likely to form. 

IV. Preliminary Curettage of the Tympanum. —If the malleus and 
incus have escaped destruction, it may be an easy matter at this stage of 
the operation to remove them with a tympanic forceps. In many cases, 
however, they have undergone complete or partial disintegration. Again, 
the necrotic remnants of the two larger ossicles may be hidden from view 
beneath masses of exuberant granulations practically filling the atrium 
and hypotvmpanic space. In removing such obstructive masses some care 
is necessary to insure against two particularly serious accidents,—viz., 
(a) injury to the horizontal portion of the facial canal, and (b) rupture or 
tearing of the capsular ligament which holds the stapes within the oval 
window. The latter accident has been the cause of more than one fatal 
case of purulent leptomeningitis. The curette having been introduced 
above and behind the obstructing mass, its edge should not touch or engage 
the inner tympanic wall,—the granulations being crowded downward 
against the floor of the hypotympanic space and thence swept out into the 
canal. We may then remove more thoroughly the remaining granula¬ 
tions,— i.e., from the floor of the hypotympanic space, the region of the 
Eustachian orifice, etc.,—particular caution being observed, however, in 
using the curette in the neighborhood of the facial canal and niche of the 
oval window. 

V. Reduction of Ridge Representing Lower Half of Posterior Canal Wall. 
—The next step is the removal of the bony spur left by the lower half of 















438 


TYMPANIC AND MASTOID OPERATIONS 


the posterior canal wall. This is sometimes spoken of as “the facial spur,” 
a term which for convenience of description shall be employed here. Our 
guide to surgical safety in this region is the bend of the facial canal (Fig. 
243). Running more or less horizontally across the inner tympanic wall, 
this canal is indicated by a linear ridge which passes backward above the 
oval window, behind which it disappears beneath the upper extremity of 
the facial spur. Beneath the apex of this spur the facial canal bends 
downward, and thence descends almost vertically to its termination in the 
stylomastoid foramen. The facial spur may therefore be safely lowered 


Fig. 244. Radical operation, after lower half of posterior canal wall has been reduced so as to appear 

as a direct continuation of the facial ridge. 



above until it has the appearance of being a continuation of the ridge 
representing the horizontal portion of the facial canal. The bend of the 
facial canal is also our chief surgical guide as to the course of the descend- 
ing portion of the facial nerve, for below the bend of the canal its direction 
is almost vertically downward. The facial nerve lies, therefore, rather 
superficially beneath the upper extremity of the facial spur, but is very 
deeply situated beneath its lower part. 

Ihe actual work of reducing the lower half of the posterior canal wall 
may be done as follows: With a straight-edged chisel the bone is removed 
in successive layers from below upward. The first one or two layers of 









THE RADICAL OPERATION 


439 


bone remo\ ed may be rather thick below, where we know the nerve to 
be deeply placed beneath our point of attack. After this, however, we 
should keep constantly in mind the direction and course of the facial 
canal, making our removal of bone only in very thin layers, and as nearly 
as possible parallel with the course of the nerve. That is to sav, if the 
chisel is made to cut in a direction at right angles to the course of the 
canal, the nerve may be completely severed, with consequent permanent 
paralysis. When the ridge has been reduced approximately to the dimen¬ 
sions we wish it to assume, it is safer to lay aside mallet and chisel, and 
complete the work with a bone curette. With a curette of fairly large 
size, we may remove any rough surfaces and at the same time lower 
the ridge gradually to the desired extent. While this work is in prog¬ 
ress the anaesthetist should constantly watch the face and immediately 
notify the surgeon of any facial twitching which may indicate that the 
nerve has been mechanically irritated. When this work is complete, 
the bone cavity should have somewhat the appearance of that shown 
in Fig. 244. 

Failure to deal adequately with the facial spur leaves a vertical promi¬ 
nence, or ridge, which more or less bars the way to the posterior end of 
the bone cavity, leaving there a space not easily reached or cared for dur¬ 
ing the period of postoperative treatment. 

VI. Removal of Outer Wall of Hypotympanic Space. —In Fig. 245 the 
hard, dense bone of the floor of the meatus is shown in striking contrast 
with the rough depression consti¬ 
tuting the floor of the tympanum. 

The hypotympanic space fre¬ 
quently contains a considerable 
amount of diploic tissue. This 
diploic tissue must be scraped 
out and the inner margin of the 
floor of the meatus removed with 
a curette. The floor of the tym¬ 
panum and contiguous portion of 
the floor of the canal must then 
be scraped to a smooth or un¬ 
broken surface. When this part 
of the operation is neglected, the 
hypotympanic floor frequently be¬ 
comes the seat of persistent granulations which prevent healing and resist 
all therapeutic measures short of a secondary operation. 

VII. Curettement of the Eustachian Orifice. —The next step of the 
operation is the very thorough curetting of the Eustachian orifice. Here 
almost invariably in chronic middle-ear suppuration is found a diseased 
mucosa. Very frequently the tube is blocked by exuberant granulations 
and it may be the seat of osseous necrosis. The treatment is a careful 
and thorough curettement. The anterior wall of the tympanum merges 



Fig. 245.—Tympanic floor. 




440 


TYMPANIC AND MASTOID OPERATIONS 



Fig. 246.— Ring 
curette. 


centrally into the funnel-shaped mouth of the bony tube. 
Into this a small curette may be introduced for some dis¬ 
tance,— i.e., 5 or 6 mm. The small ring curette shown in 
Fig. 246 is provided with sharp edges and is well adapted for 
this work. After removing any masses of granulation tissue, 
the various walls of the tube are gently scraped until the 
curette encounters smooth bare bone in all directions. Our 
purpose is not only to rid the tube of obstructing granulations, 
but also to remove completely its mucous lining. The logic 
of this treatment becomes clear when we remember that 
obliteration of the lumen of the canal is exactly what we 
wish to attain. When we have thoroughly removed the 
mucous lining and curetted the bony walls into even surfaces, 
the production of healthy granulations would seem inevitable, 
and granulating surfaces in so narrow a tube should lead 
logically to firm cicatricial stenosis. 

The writer is inclined to believe that the frequently 
reported failures of the radical operation to relieve the dis¬ 
charge from the Eustachian tube are to be explained almost 
wholly as due to a lack of thoroughness in carrying out the 
work above outlined. 

Just below and internal to the Eustachian canal— i.e. r 
separated only by its lower internal wall—is the canal for 
the internal carotid artery. While injury of the carotid 
artery is, therefore, theoretically possible, and while such 
accidents have been reported, I have personally known of 
no such cases, and believe that with reasonable care and 
gentleness in the use of the curette it is not likely to occur. 
Just above the Eustachian canal is the incomplete canal 
for the tensor tympani muscle. Removal of the plate form¬ 
ing the floor of this canal, and incidentally of the tensor 
tympani muscle itself, is followed by no untoward results 
and actually leaves a more favorable condition for prompt 
healing at this point. 

In our final survey of the work accomplished, it is neces¬ 
sary to recognize the following structures: Passing along 
the floor to the anterior tympanic wall one encounters 
first the Eustachian orifice (Fig. 247, a), immediately 
above which is the floor-plate of the tensor tympani canal 
(6). Above this, and separated from it only by a very 
limited space, is the beginning of the horizontal portion 
of the facial canal (c). This is undoubtedly the region 
in which injury to the facial nerve most frequently occurs. 
From this point the facial canal is traced as a linear ridge 
passing horizontally backward across the tympanum and 
disappearing beneath the vertical ridge representing the 



















THE RADICAL OPERATION 


411 


remains of the posterior canal wall (/). Beneath the posterior end of 
the horizontal facial ridge— i.e., just before it bends to pass downward 
beneath the posterior canal wall—is the niche of the oval window (d). 
Between the horizontal facial ridge and the hypotympanic space is the 
promontory (/i), behind which is the niche of the round window (g). 
Just above the posterior half of the facial ridge is the horizontal eleva¬ 
tion of dense, ivory-like bone, representing the anterior end of the hori¬ 
zontal semicircular canal (e). When the surgeon has sufficiently cleared 
the tympanum of its diseased mucosa and granulations, most of the 
above landmarks stand clearly revealed. I say “most” of them, be¬ 
cause I wish to note an occasional exception in the case of the oval 
window. We must trace and outline the horizontal portion of the facial 
canal in order to avoid injuring it. We know the position of the oval 


Horizontal semicircular canal (e) 
Oval window ( d ) 


Horizontal portion 
of facial canal ( c) 


Floor plate of tensor 
tympani canal (6) 


Orifice of Eustachian tube (c) ' 



Remains of posterior 
' canal wall (/) 


— Round window ( 0 ) 


Promontory ( h) 

Fig. 247.—Tympanic structures usually exposed in radical operation. 


window from its relation to the bend of the facial canal. In some case^ 
the oval niche and even the stapes itself are in plain view; in others the 
stapes is covered and the niche filled by granulations. I do not agree with 
those who believe that granulations should be removed from the oval 
niche for the purpose of investigating the condition of the stapes and 
stapediovestibular joint. If we have made a thorough preliminary exam¬ 
ination we shall have determined in advance the presence or absence of a 
labyrinthine fistula. A fistula being absent, granulations_ surrounding 
the stapes and within the oval niche may represent as distinctly a pro¬ 
tective and conservative process as do granulations upon the dura 
covering the sigmoid sinus, and in neither situation should they be 
removed The list of recorded cases of stapedial injuries leading to 
suppurative labyrinthitis has already reached an impressive number 
The writer personally knows of two deaths directly traceable to stapedial 
injury during a radical operation. So far as he knows, granulations covering 




442 


TYMPANIC AND MASTOID OPERATIONS 


the oval window do not usually indicate osseous necrosis, and do not 
interfere with postoperative healing. Furthermore, such granulations 
usually disappear spontaneously during the period of postoperative repair, 
leaving the depression of the oval window and sometimes the head of the 
stapes in plain view. 

Facial Paralysis. —Before leaving the discussion of the bone opera¬ 
tion, a word should be said as to the occasional accidental injury of the 
facial nerve. Much has been said of the danger of injuring the nerve 
during the removal or reduction of the posterior canal wall. But this 
danger—which with a careless or incompetent surgeon is quite real—is 
so obvious that most aural surgeons are forearmed against it. As a matter 
of fact, the nerve is not very frequently injured at this stage of the opera¬ 
tion. Much more frequently the injury occurs while the surgeon is using 
the curette upon some structure within the atrium. The smallness of this 
operative field, the difficulties of keeping it free of blood, and the extreme 
thinness and brittleness of the bone forming the outer wall of this part 
of the facial canal combine to place the nerve here in an exceedingly 
vulnerable position. The surgeon can not, therefore, be too careful in 
using the curette within this space. If blood collects in the wound and 
obstructs his view, he may pack the wound with gauze saturated with 
adrenalin chloride, 1 in 1000. After this has remained in position one or 
two minutes, he will usually have the advantage of a fairly dry field. 
Before proceeding with his operation, he should take time to locate defi¬ 
nitely the various tympanic landmarks, but particularly the horizontal 
portion of the facial canal. 

Temporary facial paralysis occurs in certain cases in which the nerve 
has not been exposed at any point. In such cases the paralysis is 
usually of more or less gradual development,—tjiat is, it is not complete 
when the patient recovers from the influence of the anaesthetic,—and 
must be explained as due to the pressure of inflammatory exudates upon 
the nerve or to a slight traumatic neuritis resulting from the use of 
instruments near the facial canal. The fact that a postoperative facial 
paralysis is not complete from the start is proof that the nerve has 
not been actually severed; some restoration of function may therefore 
be relied upon. In most cases the restoration is complete,—in others 
only partial. 

When the face is found completely paralyzed at the moment when the 
patient regains consciousness, the condition may cause the surgeon more 
anxiety. If he has exposed the nerve extensively and recognized it, so 
that he is sure that it has not been actually severed, he may expect rather 
confidently that the facial control will ultimately be regained. If, how¬ 
ever, he has completed his operation without any knowledge of having 
injured or exposed the nerve, and yet finds complete paralysis as the patient 
recovers from the anaesthetic, the condition is one which naturally causes 
greater anxiety, since, having injured the nerve unknowingly and to the 
extent of complete ablation of its function, he is left in doubt as to whether 


THE ZAUFAL-HEIXE OPERATION 


443 


it has actually been severed. In such cases, the anxiety of the surgeon 
can be relieved only by the degree of confidence he may feel that the opera¬ 
tion as he has performed it could not possibly have produced actual divi¬ 
sion,— i.e., loss of continuity. 

Facial paralysis following the radical operation is temporary in 
the vast majority of cases. When complete— i.e., presenting typical 
reactions of degeneration—months may elapse before any signs of 
functional improvement are discernible. It is a most distressing com¬ 
plication, and the surgeon can not be too careful to guard against its 
occurrence. 

Having completed the various steps of the operation as above described, 
it is well to scrutinize carefully the entire bone cavity for small areas of 
diseased or suspicious bone which may have been overlooked. Any rough 
points or surfaces should be made smooth, and for this purpose a spoon 
curette passed rapidly and lightly over the bone is a most effective 
instrument. Overhanging margins of cortex should be removed and the 
resulting edges made smooth. It is of considerable importance that the 
completed operation should leave the Eustachian orifice in clear view dur¬ 
ing the period of postoperative treatment and repair. In certain bones it 
will be found that the central portion of the anterior wall of the bony 
meatus bulges so prominently into its lumen as to obstruct considerably 
one’s view of the Eustachian orifice. This difficulty can usually be cor¬ 
rected by reducing the thickness of the anterior canal wall with a suitable 
curette (Richards). In the case of unusually narrow canals, the writer 
has frequently obtained very useful additional space by this method. It is 
a point of considerable importance. 

Before describing the plastic work upon the membrano-cartilaginous 
canal by which the radical operation is completed, it will be necessary to 
refer very briefly to certain variations in the method of operating upon 

the bone. 

Zaufal-Heine Operation.— Zaufal, Heine, and many aural surgeons 
of note prefer to open the antrum by the preliminary removal of the pos¬ 
terior wall and roof of the bony meatus. As Heine describes it, it is per¬ 
formed somewhat as follows: Using a small gouge, the bone is entered 
just behind the suprameatal spine and a shaving of bone from the postero- 
superior canal wall removed. If a small enough gouge is used, the outer 
three-fourths of the canal wall may be removed. The gouge is then applied 
to the contiguous portion of the roof of the meatus, and a layer of equal 
length removed. By using the gouge alternately upon the superior and 
posterosuperior walls, the pneumatic or diploic structures behind them are 
exposed, and the antrum, if of average size, is opened. When by this 
process the outer four-fifths of the posterosuperior canal wall have been 
removed, there remains the slender ‘‘bridge” of bone form?d by the 
inner margin of this wall of the bony canal. This may be removed by 
means of a small curette or chisel, as in the regular operation already 
described. When this has been accomplished, the operation reaches the 


444 


TYMPANIC AND MASTOID OPERATIONS 


stage shown by Fig. 248. The outer mastoid cortex must now be removed 
to a variable extent above, behind, and below the suprameatal spine,— 
usually to the extent indicated by the dotted line in Fig. 248. From 

this point the operation is completed by 
exactly the same steps as have been de¬ 
scribed in the previous pages. 

The above method with slight modifi¬ 
cations has been for some years in use by 
many American surgeons. The technic 
varies from that of the Zaufal-Heine 
operation chiefly in that the mastoid cor¬ 
tex and posterosuperior canal wall are 
removed simultaneously. A rather large 
gouge enters the bone behind the supra¬ 
meatal spine and removes a layer from 
the cortex above and behind the canal 
and from the posterosuperior canal wall 
at the same time. Successive applica¬ 
tions of the gouge remove shavings from 
the anterior edge of the cortex until what 
is expected to represent the posterior 
limit of the excavation is reached. In 
this way the removal of the cortex and 
of the canal wall proceed simultaneously. 
The removal of cortex progresses sufficiently rapidly to provide adequate 
space for the gradual and comparatively easy removal of the canal wall. 
Finally, when only a narrow inner margin, or “bridge,” remains of the 
posterosuperior canal wall, the operation reaches practically the stage 
shown by Fig. 242, from which point the technic does not differ from that 
already described. 

Stacke’s Operation. —Stacke’s operation proposes the exposure of 
the tympanic vault and the antrum by chiselling away first the inner 
extremity of the roof and posterosuperior wall of the bony meatus. It 
differs from the Zaufal-Heine operation in that the gouge, instead of being 
applied first to the outer margin of the canal wall and removing the same in 
layers from without inward, is applied first to the canal wall near its inner 
extremity and the bone removed in small portions from within outward. 
The steps of the operation may be described somewhat as follows: A 
postauricular incision parallel with the auricular attachment having been 
made, the anterior flap and auricle pushed forward, and the membrano- 
cartilaginous canal having been separated from the bony meatus and 
either drawn out of the canal or crowded well forward, the bone operation 
is carried out as follows: The malleus, if within reach, is removed by means 
of a tympanic forceps. The next step is the removal of the inner extremity 
of the roof of the meatus by means of a narrow gouge the end of which is 
slightly curved to facilitate its engaging the bone. With a view to protect- 



Fig. 248.—Stacke’s operation. 




ST ACRE’S OPERATION - 


445 


ing from injury important tympanic structures,—chiefly the facial canal 
and horizontal semicircular canal,—Stackers “protector,” a narrow flat 
instrument the terminal end of which is bent to an angle of 45° (Fig. 249), 
is introduced into the meatus, the end being 
carried upward into the attic. This instru¬ 
ment is held in position by an assistant. 

The surgeon then introduces his gouge, and 
chisels away the roof of the meatus from 
within outward until the superior wall of 
the vault and that of the meatus lie in the 
same plane. The protector is then rotated 
so that its terminal bent portion passes 
backward into the aditus or antrum, and 
the contiguous portion of the posterior wall 
chiselled away from within outward. This, 
of course, provides a free opening into the 
antrum by way of the meatus. Finally the 
cortex is removed over the usual area. 

Stacke’s operation, in the writer’s opin¬ 
ion, is one of the most dangerous proced¬ 
ures proposed in aural surgery. The possi¬ 
bility of injuring the facial or semicircular 
canal, either by the gouge itself or by a 
splinter of bone from the inner margin of 
the canal, can not be doubted. The use of 
the protector hardly seems to remove this 
danger, for, with the protector in place, the 
small safety space between the inner and 
outer walls of the vault is sacrificed, and 
any slip of the gouge or miscalculated force 
in the mallet blow is communicated to the 
“protector” and by it transmitted to the 
bone structures beneath. 

There is but one condition known to 
the writer in which the tympanic end of the 
posterosuperior canal seems the only safe 
point of attack for opening the antrum,—viz., when the sigmoid sinus 
literally overlies the antrum and is in actual contact, oi veiy close prox¬ 
imity, with the posterior meatal wall. This condition, though exceedingly 
rare, does exist. The writer has met with at least one such case in his 
operative experience, and has in his collection a temporal bone in v hieh 
the position of the sinus-groove is such as to render it a physical impossi¬ 
bility to have entered the antrum by any route having a starting point 
upon the outer mastoid cortex. 

Since the necessity for opening the antrum from the tympanic end of 
the meatus occasionally confronts the surgeon, the writer wishes to refer 


















446 


TYMPANIC AND MASTOID OPERATIONS 


briefly to a method of attack which he described in a paper published in 
1904, 5 and which has the advantage of absolute safety. The special in¬ 
struments required are the cutting forceps shown in Fig. 250. Two sizes 
are needed. The following description is quoted from the paper in question: 



Fig. 250.—Kerrison’s tympanic rongeur. 


Operation .—“The patient is prepared for operation and the mastoid 
cortex exposed in the usual way. The anterior flap and the auricle are 
pushed forward so as to expose the spine of Henle and entrance to the bony 
meatus, and the skin and periosteal lining separated from its posterior 
wall, roof, and floor from the entrance of the canal to its termination at 
the annulus tympanicus. The auricle is drawn forward by some form of 
retractor, preferably a strip of sterile gauze passed through the membranous 
canal. 


6 Kerrison: A Bone Forceps for Use in Tympanic Surgery; Its Value in Safeguard* 
ing the Facial Nerve, etc., Laryngoscope, May, 1904. 













TYMPANIC APPROACH TO ANTRUM 


447 


“From this point it will be necessary to work by reflected light or by 
direct illumination by means of an electric forehead lamp. 

“Before proceeding further, the fundus of the canal should be inspected. 
The remains of the drum membrane should be removed, and, if either 
malleus or incus be within view, an attempt should be made to remove it. 

If neither malleus nor incus be visible, the end of a small tympanic probe, 
bent near the tip so as to describe a right angle, should be introduced into 
the tympanum and carried upward into the vault. Should the tip of the 
probe encounter one of the ossicles blocking the entrance to the vault, 
it should be pushed backward or forward out of the way, and no attempt 
should now be made to remove it. We are now prepared for the first step 
of the bone operation. 

“In using these forceps the writer has found it easier to remove first 
the roof and posterior wall of the meatus, the mastoid cortex covering the 
antrum being removed later. 

“The small forceps (Fig. 250), with cutting edges separated and 
pointing upward, is introduced into the tympanum and carried upv ai d 
into the vault. On attempting to withdraw it, the distal cutting edge 
will be engaged by the inner margin of the roof of the meatus. The 
handles are now gradually approximated, when the blades will be felt 
to crush or cut through the bone, and may be withdrawn, bringing away 
a small portion of the upper canal wall. Having cleared the instrument 
of bone, it is again introduced into the canal and made to engage the 
roof in the notch made by the first bite of the forceps. By a repetition „ 
of this process the roof of the meatus is quickly removed. The vault is 
now exposed to view and a bent probe may be passed backward into 

the antrum. . ^ u t? 

“The next step will be the removal of the posterior canal wall. lor 

this purpose the small forceps, or the larger one if it will enter the tym¬ 
panum, is employed. It is introduced into the canal as before described 
except that its cutting edges are now directed backward toward the antrum. 
The handles are carried slightly forward in order to bring the cutting edges 
in contact with the inner margin of the posterior canal wall, which is 
rapidly removed as far outward as the spine of Henle. 

“The work just described— i.e., the removal of the superior and pos¬ 
terior canal walls—can be done quite rapidly, usually requiring not more 
than five to eight minutes. The tympanic space and landmarks, including 
the oval window, horizontal portion of the facial ridge, and prominence 
of the external semicircular canal, are now well exposed to view, and are 
kept under observation during the remainder of the operation, which 

may be completed by the usual method.” . 

This method of operating has seemed to possess the following advan¬ 
tages over Stacke’s operation: . 

1. Considerable saving of time in removing the roof and posterior 

wall of the meatus and exposing the antrum. iL . 

2. Diminished danger to important structures, from the fact that the 


448 


TYMPANIC AND MASTOID OPERATIONS 



Fig. 251 


Fig. 252 



Fig. 253 


Fig. 254. 



Figs. 251, 252, 253, 254.—Diagrams illustrating various plastic operations forming part of the 

radical operation. 

























THE RADICAL OPERATION" 


449 


bone is cat in a direction from within outward,— i.e., 
away from the stapes, facial canal, and horizontal 
semicircular canal. 

The term “radical operation” no longer refers spe¬ 
cifically to any particular method, or technic, and is 
used to describe any surgical procedure which con¬ 
verts the tympanic cavity and mastoid antrum into 
one large cavity of healthy bone, draining easily by 
way of the external auditory meatus. This mechanical 
result having been attained, the postauricular wound 
may be closed throughout. Before this can be at¬ 
tempted, however, it is necessary to adopt some form 
of plastic operation by which the membrano-cartilag- 
inous canal can be made to conform to the enlarged 
bony space. A variety of excellent meatal flaps have 
been suggested, only four of which, however, need be 
described here,—viz.: (1) Korner’s flap, (2) Panse’s, 

(3) Siebenmann’s, and (4) Ballance’s. 

The Korner Flap (Fig. 251).—Korner’s opera¬ 
tion converts the posterior wall of the membrano- 
cartilaginous , meatus into a tongue-shaped flap 
which is utilized as a partial lining for the posterior 
wall of the bone cavity. It is made as follows; 

A narrow-bladed knife (Fig. 255) is introduced into 
and through the membrano-cartilaginous meatus, 
with cutting edge directed backward, and the canal 
divided from within outward along the line of junc¬ 
tion between roof and posterior wall. Within the 
concha it is carried backward through the skin and 
conchal cartilage following a line just below and 
parallel with the conchal end of the helix. As a 
rule, it should not extend backward further than 
midway between the anterior and posterior boun¬ 
daries of the concha. The knife is then reintro¬ 
duced and a similar incision parallel with the first, 
but hugging the floor of the membrano-cartilaginous 
canal, is made through canal and concha, ending 
at a point in the concha below the termination of 
the first incision (Fig. 251, small figure). If all 
structures of the membranous canal have been 
divided, the tongue-shaped flap between the two fig. 255. —Narrow- 
incisions may now be lifted out through the meatus. b ! ad ® d kmf ® required m the 

. - . 0 • 1 jii' plastic work of the radical 

Catching the extremity of the flap with toothed operation, 
forceps and drawing it backward, the surgeon uses 

its skin covering as the part to be preserved, and carefully dissects 
from it all subcutaneous structures, including the cartilage. This dissee- 

29 



























450 


TYMPANIC AND MASTOID OPERATIONS 


tion is carried backward as far as the posterior extremities of the two par¬ 
allel incisions. The meatal and conchal cartilage thus exposed is then cut 
away. This usually completes this part of the operation. 

Prof. Korner himself no longer removes any cartilage from the concha. 
I have found this, however, a very useful procedure, as it enlarges the 
meatal opening, not enough to produce any noticeable deformity, but it 
does give valuable space through which to carry out postoperative treat¬ 
ment. Some operators, before closing the posterior wound, suture the 
meatal flap back against the anterior flap of the postauricular wound with 
a catgut suture. Personally the writer has not found this necessary. After 
cutting the flap, he has proceeded to close the postauricular wound, either 
by interrupted silkworm-gut sutures, or by the metal clamp sutures. The 
concho-meatal flap is then carried to its place against the posterior wall 
of the bone cavity and held there by a firm packing of iodoform gauze. 

The Panse Operation (Fig. 252).—This operation makes of the pos¬ 
terior wall of the membrano-cartilaginous canal two flaps,—a superior 
and an inferior. The narrow knife is introduced, as before, through the 
membranous canal, and a longitudinal incision made through the centre 
of its posterior wall. This incision includes the cartilage .and is carried 
backward into the concha, usually to its mid-point (Fig. 252). The knife 
is now inserted at the posterior extremity of the first incision, and two 
vertical incisions— i.e., one upward and one downward—are made at 
right angles to the first. This T-shaped incision provides for an upper and 
a lower flap. The skin is now dissected up from each flap, and the conchal 
and meatal cartilage so exposed is excised. When these flaps have been 
placed in position, and held there by catgut sutures or preferably by care¬ 
ful packing of the wound, they form a nucleus for the future epidermal 
lining of the roof, anterior wall, and floor of the bony cavity. The pos¬ 
terior wall is not provided for, but may be covered later by skin-grafts, or in 
successful cases is covered by the rapid spread of epidermis from other parts. 

The Siebenmann Flap (Fig. 253) up to a certain point closely resem¬ 
bles that of Panse. The membrano-cartilaginous canal is divided by a 
longitudinal incision which passes through the centre of its posterior wall, 
but ends at the anterior margin of the conchal cartilage. From the pos¬ 
terior extremity of this incision, two short incisions extend, one upward 
and backward and the other downward and backward (Fig. 253). This 
provides for three flaps,—viz., a broad upper flap (a), a lower flap (b), and 
a short pointed or triangular flap (c). The skin covering each of these 
flaps must now be dissected up and the underlying cartilage removed. 
This method offers the advantage over Panse’s operation that the short 
posterior flap provides a covering of skin for the posterior margin of the 
meatus, and a.point from which epidermization may proceed over the 
posterior wall of the bone cavity. 

Besides the above there are a number of excellent plastic methods, includ¬ 
ing that of Ballance, of London (Fig. 254), which is particularly suitable 
when it is desirable to secure considerable enlargement of the orifice of the 
membranous meatus. Any of these operations will give favorable results 


THE RADICAL OPERATION 


451 


in suitable cases. Another modification, which has come to the writer’s 
knowledge since the accompanying illustrations were drawn, is the method 
introduced by Briihl. Bruhl’s operation is a modification of Panse’s,— 
i.e. y the T-incision of Panse is supplemented by two parallel incisions 
passing backward through the concha and providing a short Korner-like 
flap. Bruhl’s operation is therefore a combination of the salient features 
of the Panse and Korner methods. 

From the foregoing description it will be seen that in appropriate 
cases the completion of the bone operation is immediately followed by 
the plastic work upon the membranous canal and complete closure of the 
postauricular wound. There are, however, several conditions in the pres¬ 
ence of which it is safer, in the writer’s opinion, to postpone the closure 
of the wound. These may be mentioned in the following order: (a) Ex¬ 
posure plus injury— i.e., tearing or puncture—of the dura at any point; 
(b) extensive exposure of the sigmoid sinus; (c) mid-cranial epidural 
abscess; perisinous abscess; and (d) large cholesteatomatous masses within 
the antrum and adjacent mastoid spaces. However thorough may have 
been our removal of cholesteatomata, it is safer to keep under inspection 
the surfaces from which they have been removed until these are completely 
covered by healthy granulations. 

I am aware that many distinguished surgeons will not agree with me 
in regarding all the conditions above referred to as contra-indications 
to the immediate closing of the wound. Any of the above conditions, 
however, may lead to serious complicating lesions, and it seems to me 
more in accordance with surgical principles to keep the wound open until 
all doubtful areas are covered by a layer of healthy granulations. 

When the bone operation results in a cavity whose walls in all direc¬ 
tions are formed of healthy bone, the plastic work upon the canal and 
closure of the posterior wound should form part of the original operation. 

Postoperative Treatment. —The postoperative treatment is almost 
or quite as important as the operation itself. That is to say, the surgeon 
who operates—no matter how carefully—and leaves the after-care of his 
cases to others will surely obtain but poor average results. 

Ordinarily the first dressing should not be changed, or at least the 
gauze packing within the bone cavity should not be removed, until the 
third or fourth day after the operation. In some cases removal of the 
first dressing reveals a practically dry wound, in which cases the bone 
cavity should at once be repacked, this time with plain sterile gauze. If, 
on the other hand, the dressing is found saturated with serum or pus, the 
cavity should be carefully wiped dry with pledgets of sterile cotton, dusted 
with dry boric acid powder, and then firmly packed with strips of sterile 
gauze. After removal of the first packing, the dressing should be changed 
at least as often as on alternate days. In some cases it is advantageous, 
or even essential, to change the dressings daily. 

It is important that at each change of dressing the wound should be 
made as nearly as possible dry before the gauze is replaced, and that the 
space representing the original tympanic cavity should be packed as tightly 



452 


TYMPANIC AND MASTOID OPERATIONS 


as possible without exerting dangerous pressure upon the facial canal. 
The necessity for tight packing is clear when we remember that our pur¬ 
pose is to retard the growth of granulations beyond the thinnest possible 
layer covering the tympanic walls, and to encourage the rapid spread of 
epidermis from the flaps partially lining the bone cavity. Experience has 
taught that the process of epidermization progresses not only more surely, 
but also more rapidly, under a tight packing than in a lightly packed 
cavity. In a loosely packed bone cavity, granulations are likely to grow 
rapidly at certain points and effectively check the spread of the epidermis 
which otherwise would soon line its walls. 

When, in spite of our efforts at prevention, the rapid growth of granu¬ 
lations in certain regions interferes with the process of epidermization, some 
means of removing them must be found. The use of strong solutions of 
nitrate of silver as a means of reducing redundant granulations has never 
in my hands given satisfactory results. When granulations must be re¬ 
moved, we shall save time and accomplish our work more effectively by 
means of a curette. The bone cavity should be packed with sterile gauze 
saturated with a 10 per cent, solution of cocaine. After this has been 
allowed to remain in position ten minutes, the offending granulations may 
be removed with a curette without discomfort to the patient, and usually 
without troublesome hemorrhage. The rapid reproduction of the granu¬ 
lations should be guarded against by very careful and firm packing. 

There are certain cases—particularly those in which cholesteatomata 
have been present—in which during the first weeks following the operation 
the wound at each change of dressing is found to be bathed in a purulent 
secretion of very offensive odor. I have known such cases in which no 
physical evidences of remaining osseous necrosis could be found, and which 
ultimately went on to perfect healing. Peroxide of hydrogen is an efficient 
temporary deodorizer in such cases, but neither the peroxide, bichloride 
of mercury, nor wet dressings of permanganate of potassium prevent the 
return of the odor. I have found that dry boric acid powder properly used 
will correct this condition more quickly and with greater certainty than 
any other agent. It should not be introduced by a powder-blower, but 
carried into the wound in considerable quantity upon the blade of a spatula 
or upon any flat dull instrument. The bone cavity having been half filled 
with the powder, a strip of sterile gauze should be firmly packed against 
it. The action of dry boric acid powder used in this way is threefold,— 
i.e., (a) it effectually deodorizes the wound, (b) it reduces the amount of 
pus secreted, and (c) it seems to exert an inhibitory influence upon the 
growth of new granulation tissue. 

Certain cases which do not respond favorably to the measures above 
outlined will occasionally do well under the following treatment: The 
wound, having been wiped dry of fluid pus, is irrigated with a warm solu¬ 
tion of boric acid and again dried. The bone cavity is then completely 
filled with dry boric acid powder, and the canal protected by a pad of 
sterile cotton placed in the concha. Each day the powder is removed by 
irrigation, the cavity carefully dried, and again filled with boric acid powder. 


POSTOPERATIVE TREATMENT 


453 


I have had under my care cases which healed perfectly under this treat¬ 
ment, which I had believed would eventually require a secondary operation. 

Use of Dakin’s Fluid .—A method of treatment which in my experience 
has shown many positive advantages in cases in which the requisite care 
can be assured, is carried out as follows: On the second or third day after 
operation, all gauze packing is discontinued. The nurse is instructed every 
two hours to syringe the ear with fresh Dakin’s Fluid (i.e., of not over 48 
hours’ standing); after syringing, the patient is to lie down and the operated 
ear, turned upward, is filled with Dakin’s Fluid, which is allowed to remain 
20 minutes. Between such treatments the ear is protected with a bit of 
sterile absorbent cotton in the concha (not in canal). After 3 or 4 days ol 
this treatment, the ear should be surgically clean and free from all exuber¬ 
ant granulation. From this point the routine is modified as follows. Once 
daily the irrigation and soaking with Dakin’s Fluid is carried out. Following 
this the bone cavity is carefully filled with chlorazine paste which is pro¬ 
tected with sterile cotton and remains until the next daily dressing. 

The above is of course nothing more than an application of the Carrell 
theory and treatment to the certainly not sterile bone cavity of a radical 
operation. This theory is based on the hypothesis that frequent flushing 
with Dakin’s Fluid of an open infected wound will produce thorough steril¬ 
ization; that chlorazine paste, though not sufficiently bactericidal to in¬ 
sure sterilization in the first place, may in the second be depended upon to 
prevent reinfection. 

Chlorazine paste is made in conformity with a formula approved in the 
laboratory of the Rockefeller Institute, New York. It is properly pre¬ 
pared for the profession by the Abbott Laboratories of Chicago. Its 
application calls for care, and it requires a syringe, preferably glass, with a 
long, slender, pipette-like extremity, so curved that the paste may be deliv¬ 
ered to any part or recess of the bone cavity. 

The advantages of this treatment are: (1) Bone cavity is kept surgically 
clean. (2) Masses of exuberant granulations do not form. (3) Epidermization 
begins sooner and simultaneously in different parts of the wound. (4) 1 he 
treatment is practically without pain or discomfort to the patient. 

Skin-grafts .—The use of skin-grafts at the time of the primary opera¬ 
tion is not advisable, for the following reasons,—viz.: (1) Skin does not 
adhere normally to bare bone; the grafts would, therefore, become effective 
only after islands of granulation had formed beneath them. (2) Minute 
foci of septic matter overlooked at the time of the operation, becoming 
encapsulated between the u graft and the underlying bone, might give 
rise to serious local osseous necrosis. (3) Minute bone defects leading to 
the meninges might, under the influence of germs confined under a skin- 
graft, lead to intracranial infection. When, however, the cavity has 
become lined with a layer, however thin, of healthy granulations, the use 
of skin-grafts is not only safe but may hasten very materially the final 
healing. Usually a favorable time for applying skin-grafts is from ten 
davs to two weeks after the primary operation. 


454 


TYMPANIC AND MASTOID OPERATIONS 


The anterior surface of the thigh affords a convenient area from which 
to remove the skin. Large Thiersch grafts—as large as can be obtained— 
are removed with a wide-bladed razor, and slid from its surface upon 
specially devised spatulse (Ballance), upon which they rest, cut surface 
downward, until they are introduced into the wound. In cutting the grafts, 
the thinnest possible layer of skin should be removed. Each graft is 
placed in position by sliding it from the spatula on which it rests to the 
surface it is intended to cover. When all the grafts are in position, small 
pads of sterile cotton or gauze are placed in contact with them, and pres¬ 
sure maintained by very careful packing of the intervening wound space. 

When a single large graft has been obtained, it may be introduced in 
the following way: The end of a strip of sterile gauze is folded back and 
forth into a thick pad which is approximately large enough to fill the cavity 
completely; over this pad the skin-graft is folded, skin surface inward, 
cut surface outward. The whole is then introduced into the bone cavity 
and packed tightly. Unless the condition of the wound requires its 
removal earlier, the gauze packing should be left a full week undisturbed. 
When finally the gauze is removed, part or all of the grafts may remain in 
position, or practically all may come away, leaving, however, small islands 
of epithelium from which there is a rapid growth of skin over the entire 
cavity. The use of skin-grafts in certain cases hastens healing materially. 
Whether their routine use would greatly shorten the average period of 
postoperative repair is a question not yet settled. 

In papers dealing with the after-treatment of the radical operation, 
much has been said of the frequent failure to obtain healing or cessation of 
discharge, from the Eustachian tube. To correct this condition various 
measures have been advised, among which is the use of small skin-grafts 
placed over the anterior tympanic wall, the centre of the graft being 
carried into the Eustachian orifice by the pressure of carefully applied 
gauze packing. If the tube still retains its mucosa, however, or is the seat 
of a suppurative process, I cannot see how this or any other non-operative 
measure can have any influence in bringing about permanent closure. 

To epitomize: In the case of a persistent discharge from the tympanic 
orifice of the Eustachian tube, the writer can see only one logical method 
->f treatment,—viz., a small, sharp curette should be introduced as far as 
it will go into the canal, and not only granulations, but also every vestige 
of mucous membrane should be removed from its lumen as far as the curette 
will reach. When this is successfully performed, it would seem logical to 
expect the formation of healthy granulations, which in so small a space 
should result in firm cicatricial stenosis. 

No definite statement can be made as to the time in which healing 
will take place in any particular case. Final healing may occur in very 
favorable cases in from four to five weeks, or it may require ten weeks or 
more of constant care. Eight weeks will probably represent about the 
average duration of postoperative treatment before the wound is perfectly 
dry and lined everywhere with a covering of skin. 


THE HEATH OPERATION 


455 


The Influence of the Radical Operation upon Hearing is so 
variable that one is never justified in making definite promises to the 
individual patient. Assuming the cochlea to be intact and functionating, 
and finding the tympanic cavity filled with granulations or the auditory 
canal blocked by polypi, one is naturally more hopeful as to the probable 
influence of the operation upon the auditory function than in a case in 
which such obvious obstacles to sound conduction do not exist. Not 
infrequently, however, very fair and useful hearing power coexists with 
other conditions imperatively demanding the radical operation. In such 
cases the hearing may be improved, may remain undamaged, and in some 
instances is undoubtedly reduced as a result of operative intervention. 
My own experience is that the hearing is oftener improved or unchanged 
than curtailed by the operation. The occasional cases in which serious 
loss of hearing has resulted from it have led to attempts to modify the 
operation so as to secure more uniform conservation of hearing. Of these 
the most widely known is that of Mr. Charles J. Heath, of London. 

The Heath Operation for Chronic Middle-ear Suppuration.— 
This operation is based upon its author’s theory that in the great majority 
of cases chronic middle-ear suppuration is the result of disease located 
within the antrum; and that the fluid products of antrum disease, draining 
by way of the aditus into the tympanum proper, act as constant irritants 
upon the tympanic and tubal mucosa, thereby perpetuating the suppu¬ 
rative process within the middle ear. From this hypothesis he draws the 
deduction that the antrum is the logical point of attack, and that, if we 
can eliminate the focus of disease there, the tympanic lesion will undergo 
spontaneous cure, or at least may be controlled by measures applied 
through the auditory meatus. 

Operation . 6 —The first steps are precisely the same as in the radical 
operation. The antrum is uncovered, granulations blocking the aditus 
are removed by means of a curette, and the aditus is then temporarily 
closed by a pledget of sterile cotton. Diseased structures within the an¬ 
trum and adjoining cells are dealt with in the usual way. The posterior 
wall and roof of the bony meatus are next removed from without inward 
to a point near their inner extremity, the annulus tympanicus being re¬ 
tained to support what remains of the membrana tympani. This brings 
the tympanum, or drum membrane, within easy reach, and any granula¬ 
tions or polypi protruding through the perforation are carefully removed. 
A specially constructed cannula, connected by rubber tubing with an air 
bulb, is then adjusted within the aditus and a forcible air-current pro¬ 
pelled through aditus, vault, and atrium,—the purpose being to expel 
into the meatus any residual pus or other inflammatory products remain¬ 
ing within the tympanic cavity. 

A plastic operation upon the membrano-cartilaginous meatus is then 


6 Heath: The Cure of Chronic Suppuration of the Middle Ear without Removal 
of the Drum or Ossicles or Loss of Hearing, Lancet, August 11, 1906. 



456 


TYMPANIC AND MASTOID OPERATIONS 


performed as for a radical operation, and the postauricular wound sut¬ 
ured. A large rubber drain is introduced through the enlarged meatus 
into the antromastoid cavity. This completes the operation. 

The after-treatment consists of frequent changes of the dressing and 
periodic inflation of the tympanum by cannula introduced into the aditus. 

The advantages claimed are that the ossicles are not sacrificed, and 
that the tympanic membrane is frequently reproduced, with consequent 
preservation, and in some cases appreciable improvement, of hearing. 

While the Heath operation has been tried by surgeons in all parts of 
the world, the results have not been sufficiently favorable to bring univer¬ 
sal recognition of its value. Apparently it is applicable to a comparatively 
small class of selected cases. That it is not available in a majority of the 
cases for which the radical operation is employed is made clear by a con¬ 
sideration of the following facts,—viz.: (a) In a very large percentage of 
cases requiring operation the malleus and incus are necrotic, and the con¬ 
dition of the drum membrane beyond repair, in which case their preserva¬ 
tion would hardly be in accord with sound surgical principles; (b) the 
presence of a marginal perforation, now recognized as one of the indica¬ 
tions for surgical intervention, means partial loss of the annulus tympanicus 
■—a condition which precludes the possibility of a regenerated drum mem¬ 
brane. Clearly, therefore, many of the conditions which the radical opera¬ 
tion is designed to meet would not be relieved by the Heath operation. 

Bondy’s Operation. —Dr. G. Bondy, of Vienna, has also devised a 
substitute for the radical operation, having for its purpose the conserva¬ 
tion of the ossicles and thereby the preservation of the hearing. Naturally 
it is applicable only to cases in which the ossicles are sound and the con¬ 
tinuity of the ossicular chain intact. 

Operation .—The cortex is exposed as for a radical operation, but with 
the difference that the membrano-cartilaginous canal is not at this stage 
separated from its attachment to the walls of the bony meatus. Leaving 
the membranous canal undisturbed insures against any injury to tympanic 
structures at this stage of the operation. The antrum is now uncovered 
and all diseased structures are removed. The aditus is enlarged so as to 
provide the freest possible communication between the tympanic vault or 
attic in front and the antromastoid cavity behind. The membranous canal 
is now separated from the walls of the bony meatus, and the posterosupe- 
rior canal wall chiselled away. This removal includes the inner marginal 
“ bridge, ” which gives support chiefly to Shrapnell’s membrane. The outer 
wall of the tympanic vault is carefully and thoroughly removed, this being- 
regarded as a feature of the operation particularly essential to a successful 
result. The facial “spur, ” or ridge, formed by the lower part of the posterior 
canal wall, is lowered almost to the line of attachment of the membrana tensa. 
Granulations or diseased structures in the vault above the head of the mal¬ 
leus and body of the incus are removed, but the ossicles themselves are not 
disturbed. The operation, therefore, proposes the removal of all diseased 
structures from antrum, aditus, and tymapnic vault, but preserves the 
ossicles and whatever remains of the tense membrane. The operation is 



Fig. 250.—Instruments essential in the operation of ossiculectomy 


















































OSSICULECTOMY 


457 


concluded, as is the usual radical, by a plastic operation upon the membrano- 
cartilaginous canal (Siebenmann flaps) and closure of the posterior wound. 

Bondy has operated on a number of cases by this method, with successful 
results as measured both by cessation of discharge and the preservation of 
hearing. He regards it as indicated in most cases requiring operations in 
which the continuity of the ossicular chain can be assumed, and the hear¬ 
ing distance for speech in low conversational tones is two meters or over. 

Streit’s Operation . 7 —A similar operation has recently been proposed 
by Dr. Hermann Streit, of Konigsberg. Advising rather different opera¬ 
tive technic, he secures a mechanical result which, so far as the bone opera¬ 
tion is concerned, differs little from that of Bondv’s operation,— i.e., antrum 
and adjacent mastoid cells exposed, posterior canal wall lowered nearlv to 
the line of attachment of the tense membrane, and outer wall of vault thor¬ 
oughly removed, the ossicles and membrana tensa being undisturbed. He 
performs no plastic operation upon the membranous canal, which is simply re¬ 
placed in position and held by tamponade. Omission of the plastic part of the 
operation does not appeal to the writer as promising good average results. 

An interesting discussion of the relative merits of some of the proposed 
modifications of the radical operation will be found in a paper by Dr. 
Geo. L. Richards. 7 ® 

Ossiculectomy.—The indications for this operation cannot be re¬ 
duced to exact statement. There is no possible means of determining 
definitely, in any case of chronic middle-ear suppuration of long standing, 
that areas of necrosis or foci of infection do not exist in regions beyond the 
reach of surgical measures confined to the tympanic vault. The value of 
ossiculectomy must, therefore, depend very largely upon the experience and 
judgment of the individual surgeon. Personally the writer has never seen 
a case in which he felt justified in advising it. 

The most promising cases for ossiculectomy are those in which with 
only moderate discharge, there are evidences of ossicular necrosis,— i.e., 
ossicles or ossicular remnants upon which bare, rough bone can be detected 
by the tympanic probe. Again, in certain cases in which the ossicles re¬ 
main intact, their presence seems to interfere with drainage from the tym¬ 
panic vault. Even in such cases, however, ossiculectomy should be under¬ 
taken only with the understanding—in which the patient should share— 
that a final resort to the radical operation may become necessary. 

Preparation. —The auricle and parts about the ear are scrubbed 
with soap and water and dried. The canal should be filled with hydrogen 
peroxide, which five minutes later is removed by irrigating the canal and 
tympanum with a solution of carbolic acid, 1 in 300. The fundus of the 
canal— i.e., tympanum—is packed with a strip of sterile gauze saturated 
in a 10 per cent, solution of cocaine. This is allowed to remain in position 
ten minutes. The tympanic mucosa, being exposed through the usually 
large perforation, is subject to the local influence of the drug. Removal of 


7 Streit: Monatschrift f. Olirenheilkunde, Bd. 45, Hft. 4. 
7a Richards, Geo. L.: Annais Otol., Sept. 1911. 






458 


TYMPANIC AND MASTOID OPERATIONS 


the gauze, therefore, leaves the tympanum locally anaesthetic, and the 
operation should be commenced at once. 

The instruments required (Fig. 256) are cotton applicators, ten or 
twelve in number, with cotton already attached; a sharp myringotome; a 
small angular knife; tympanic forceps; right or left incus hook according 
to ear operated on; tympanic ring curettes. 

Operation. —We shall assume that any obstructing granulations have 
been removed at a previous sitting. Supposing the perforation to be a 
central one leaving a fairly wide margin on all sides, the operation is begun 
as follows: The myringotome is introduced anteriorly near the periph¬ 
ery and just in front of the short process, the cutting edge being directed 
downward. The membrane is then carefully incised along its peripheral 
margin, the knife being carried at first downward along its anterior attach¬ 
ment, then backward and finally upward along the posterior segment of 
the tympanic ring to the posterior fold (Fig. 257). The knife now cuts 

through the posterior fold, follows the margin of 
the Rivinian notch, and cuts its way forward and 
downward to unite with the starting-point of 
the original incision in front of the short process. 
This incision should have divided the anterior, 
lateral, and posterior ligaments of the malleus. 
The malleus may now be grasped just below the 
short process with a tympanic forceps, and drawn 
downward and removed through the canal. Should 
the incus have been displaced backward by this 
manipulation, the angular bend of the incus hook 
should be carried horizontally backward along the 
floor of the aditus, then rotated forward, bringing 
the ossicle with it. The incus is then grasped by the forceps and removed. 

The canal may be again irrigated, this time with warm boric acid or 
normal salt solution. It is then dried, and the canal lightly packed with a 
strip of sterile gauze. 

Obviously the technic in removing necrotic ossicles will vary according 
to the condition of the ossicles, the part of the drum membrane remaining, 
the situation of marginal perforations, etc. When the normal connection 
persists, or pathological adhesions have formed, between the stapes and 
incus, care must be observed to avoid rupture of the stapedial capsular 
ligament. In such cases the small angular knife may be of use. In many 
cases, however, the connection between incus and stapes will have been dis¬ 
solved by the pathological process which the operation is intended to relieve. 

Many surgeons have recorded their varying results from this operation. 
One of the most interesting and instructive papers on the subject is that by 
Hunter Tod, 8 of London. Tod operated upon 120 cases with a result of 
52 per cent, of complete cures, and 30 per cent, of the cases improved. 

8 Hunter Tod: Value of Ossiculectomy in Chronic Middle-ear Suppuration, Lancet. 
Sept. 3, 1910. 









THE MOSETIG-MOORHOF OPERATION 


459 


Plastic Operations for Closing a Postauricular Opening Following 
the Radical Operation. — A fortunately rare sequence of the radical 
operation is the presence, after healing has taken place, of a permanent 
opening behind the ear. This opening leads into the antrotympanic 
cavity resulting from the bone operation, and from its .margins the skin is 
continuous over the entire cavity. I say the entire cavity is covered with 
skin, for the reason that, unless complete epidermization has taken place, 
the plastic operation we are about to consider is not indicated. 

Mosetig-Moorhof Operation. —This operation proposes the utili¬ 
zation of a flap to be obtained from the tissues immediately below the 
opening to be closed. The entire operative field— i.e., the antrotympanic 
cavity, auricle, and region behind the ear—is sterilized with the greatest 
care. Upon the skin just below the opening, a flap is marked with the 
point of the knife in shape conforming to, but a little larger than, the open¬ 
ing to be closed. Usually this flap is either oval or round in contour, and 
the incision takes the form of an incomplete circle or ellipse (Fig. 258). 
The terminal points of this incision are placed at a level l 1 ^ to 2 mm. 
below the lower margin of the opening to be closed. The incision delineat¬ 
ing this flap is carried down to the periosteum. An incision is then made 
around the margin of the opening except opposite the base of the flap 
outlined below, and from this marginal incision the skin is dissected up for 
about 1 mm. (Fig. 259). The flap is now dissected up from the under¬ 
lying periosteum, leaving, however, its attachment at the base undis¬ 
turbed. The flap is then turned upward and inverted so that its skin 
surface becomes part of the lining of the cavity thus closed in. The edges 
of the flap are sutured to the prepared margins of the opening by interrupted 
silk sutures or, if skin-grafts are to be used, by fine catgut sutures. The 
skin around the denuded area from which the flap has been taken is then 
elevated and drawn together and sutured (Figs. 260 and 261). 



Heine calls attention to the fact that the tissues immediately below 
the opening may be largely cicatricial and therefore give little promise of 












460 


TYMPANIC AND MASTOID OPERATIONS 


a flap capable of re-establishing its nutrition. In such cases he has modi¬ 
fied the operation to the extent of obtaining his flap from the tissues 
immediately behind the opening. This is a rational procedure, and one 
to be borne in mind. 

Politzer states that in certain cases in which he has performed this 
operation he has witnessed a rather free growth of hair into the antro- 
tympanic cavity, this occurring in some cases in which there had been 
little hair in the region from which the flap was taken. The operation is, 
however, a rational one which should give good results in properly selected 
cases,— i.e., those in which the opening is not very large, the bone cavity 
completely epidermized, and the tissues surrounding the opening healthy. 

The Passau-Trautmann Operation. —The steps of this operation 
are clearly indicated in the accompanying illustrations (Figs. 262 to 265). 
Two semicircular incisions are made, one behind and the other in front of 
the opening (Fig. 262). The two crescentic flaps thus formed are then 
dissected up, the posterior from the periosteum, the anterior from the 
periosteum or, if the anterior margin of the opening is near the postauric- 
ular sulcus, from the perichondrium covering the posterior surface of the 
concha. These crescentic flaps are then inverted and their edges approxi¬ 
mated (Fig. 263) and finally sutured (Fig. 264). These first sutures are of 
the finest catgut. The skin surfaces of the flaps, thus inverted, unite to 
form part of the lining membrane of the outer wall of the cavity thus 
closed in. This leaves the outer, raw surface of the flaps exposed. In 
order to cover in this denuded area, the surrounding skin is elevated, and 
then drawn together and united by means of interrupted silk sutures 
(Fig. 265). 



Figs. 262, 263, 264, 265. —Successive steps of the Passau-Trautmann operation. 

The operations described above should fulfil admirably their chief 
purpose,— i.e., the closure of a postoperative opening after complete 
epidermization has taken place. This, however, subjects the patient to 
the prolonged discomfort incident to this very trying postoperative con¬ 
dition. In my own operative experience this particular defect has not 



THE PASSATJ-TRAUTMANN OPERATION 


461 


occurred as a result of the radical operation. I am, therefore, led to believe 
that except in cases of grave constitutional disease or dyscrasia it is usually 
preventable. By this I do not mean to imply that breaking down of the 
postauricular wound is always preventable, but simply that we are usually 
able to determine, very shortly after the original radical operation, that 
postauricular healing is not progressing satisfactorily, and that permanent 
closure is, therefore, not likely to be secured. Under such conditions I 
believe that this is the proper time to forestall or correct this defect, and 
that we subject the patient to very considerable and needless discomfort 
and hardship if we leave this corrective work to be taken up only after 
healing shall have become complete. 

As aural surgeon to the Willard Parker Hospital for Infectious Diseases, 

I have repeatedly been obliged by the urgency of the aural symptoms to 
perform a radical operation upon children shortly after their discharge 
from the scarlatina wards of that institution. In such cases sloughing out 
of the sutures and imperfect union along the suture line constitute a not 
unusual experience. For this condition I have found reopening and re¬ 
suturing of the wound quite useless, the untoward sequence of events 
just described being usually repeated. To meet this difficulty, I have 
employed a very simple operation, which I shall take time to describe 

briefly. 

Author’s Operation for Preventing or Closing Postauricular 
Fistula Following the Radical Operation. —Usually there is little 
difficulty in obtaining firm union throughout the upper and lower thirds 
of the postauricular wound, the point at which the wound usually breaks 
down being near the centre. As the operation is equally effective for a 
postauricular fistula of longer standing, the illustrations are drawn as for 

the correction of the latter condition. 

The head should be shaved as for the original radical operation and 
the parts carefully sterilized by the usual method. The wound should be 
reopened by incisions conforming to the following plan: If the breaking 
* down of the suture line is of recent occurrence, so that no considerable 
loss of tissue has occurred, the wound is simply reopened or incised along 
the recent suture line, and the edges of the lips of the wound are freshened 
and made straight by removing with knife or scissors the surface layer of 
cicatricial or devitalized tissue. If the condition is of longer standing and 
has resulted in a rounded opening of considerable size (Fig. 266), two 
incisions should be made following the lines indicated in Fig. 267. That is 
to say, beginning one’s first incision at a point falling within the old suture 
line and a half inch to three-quarters of an inch below the lower border of 
the fistula, it is carried upward to the posterior border of the opening and 
thence upward to a point at an equal elevation above its upper margin. 
The two terminal points of this incision are next united by a second in¬ 
cision anterior to the first and passing through the anterior margin of the 
opening (Fig. 267). The skin and subcutaneous tissue included between 
these incisions above and below the opening are then removed. A third 


462 


TYMPANIC AND MASTOID OPERATIONS 


incision, longer than the first two, slightly curvilinear, and roughly parallel 
with and three-quarters of an inch to an inch behind the first incision, is 
then made, passing through the periosteum to the bone. \\ ith the Lang- 
enbeck elevator (Fig. 212), the tissues are carefully separated from the 
bone from the long posterior incision forward to the wound which we desire 
permanently to close. In doing this, great care should be taken to avoid 
injuring the periosteum. This absolutely relieves all tension. The post- 
auricular wound is now reclosed with interrupted silk or silkworm-gut 
sutures. Sterile gauze is introduced into the shallow wound resulting from 
the long posterior incision (Fig. 268). The dressing should be changed 



Fig. 266. Fig. 267. Fig. 268. 

Figs. 266, 267, 268.—Author’s operation for preventing or closing postauricular opening following 

radical operation. 


daily. Should stitch abscesses develop, or should firm healthy union along 
the suture line fail, this does not foretell failure in the final result. The 
stitches should be removed. The posterior supplementary wound should 
now be used to maintain proper apposition of the lips of the wound cover¬ 
ing the old defect or opening. This of course is done by packing a sufficient 
amount of sterile gauze into the posterior (supplementary) wound to push 
the soft parts forward and hold the anterior wound closed without sutures 
and without strain. This, if the dressings are carefully looked after, will 
result in rapid, firm closure of the wound immediately behind the ear, 
after which we have simply to deal with the posterior, supplementary 
wound, which always heals fairly quickly by granulation. 

One objection which may be raised to this procedure is the scar which 
inevitably marks the site of the supplementary wound. If this falls within 
the area of hair growth, it may in a boy be made noticeable by the 
absence of hair in the scar line. Such a scar, if conspicuous, could be 
easily removed by the very simple procedure of excising the scar tissue 
and uniting the lips of the resulting wound. 

In my hands this operation has been an effective means of preventing 
a permanent postauricular opening in certain cases in which it otherwise 
■would have been inevitable. 













CHAPTER XVI. 


« 

labyrinthectomy; the radical labyrinth operation; sur¬ 
gical DRAINAGE OF THE LABYRINTH. 

Indications. —In the present state of our knowledge, there are but 
few conditions which may be considered positive indications for opening 
the labyrinth. Among these may be included the following: 

(a) Chronic middle-ear suppuration with history of past attack of 
acute vestibular inflammation (nystagmus, vertigo, etc.); the diseased 


Ampullar end of 
anterior vertical canal 


Horizontal portion 
of facial canal 



Oval window 


Ampullar end of 
horizontal canal 

Descending portion 
of facial canal 


Fig. 269.—Section through tympanum, aquseductus Fallopii, and ampullar ends of horizontal 
and anterior vertical canals,—showing the relation of latter to oval window and horizontal portion of 
the facial canal. 


ear being absolutely deaf and showing complete absence of caloric irrita¬ 
bility; persistent aural discharge. This condition obviously calls for sur¬ 
gical relief, and, since any surgical intervention falling short of the com¬ 
bined radical and labyrinth operations adds to, rather than lessens, the 
patient’s danger, the labyrinth operation must be regarded as positively 
indicated. It is in the latent stage of suppurative labyrinthitis that the 
labyrinth mav be opened with least risk to the patient. Prognosis is, 
therefore, fairly good. 

(b) Acute stage of diffuse suppurative labyrinthitis plus definite and 
persistent symptoms of meningeal involvement. Phis is a grave condition 

in which the patient’s life is in constant jeopardy. The operation is called 

463 









464 TREATMENT OF SUPPURATIVE LABYRINTHITIS 


for in hope of preventing further serious involvement of the meninges. 
Prognosis exceedingly doubtful. 

(c) Symptoms of acute diffuse suppurative labyrinthitis coming on 
shortly after a radical or other tympanic operation, and presumably indi¬ 
cating an accidental rupture of the capsular ligament of the stapes. Such 
lesions are known to produce so high a death-rate that no time should be 
lost in opening and draining the vestibule. Prognosis, in early operation, 
— i.e., before meningeal infection has occurred,—fairly good. When 
operation is delayed until leptomeningitis is obviously present, the chances 
are against recovery. 

(d) Discovery during a radical operation of an open oval window 
(stapes being absent or the capsular ligament ruptured) through which 
pus exudes. 

(e) Fistulse, due to necrosis in any part of the inner wall of the atrium, 
— i.e., vestibular windows or upon promontory,—through which pus can 
be seen to escape. 

Among the physical conditions which in themselves constitute a reason 
for opening the labyrinth, a fistula in the outer wall of the horizontal 
semicircular canal is not included. The writer shares the opinion of those 
(Hinsberg, Panse, Heine, and others) who believe that a fistula in this 
location may, though rarely, represent a distinctly circumscribed labyrinth¬ 
itis, from which the patient not infrequently makes a spontaneous recovery. 
In such cases the question of operation should be decided only after a care¬ 
ful functional examination,— i.e., by the presence and character of symp¬ 
toms pointing to diffuse suppurative labyrinthitis. 

Before attempting to describe the various methods of operating upon 
the infected labyrinth, it may be well to refer very briefly to certain dif¬ 
ferences of opinion as to the mechanical results which the operation should 
aim to secure. 

Free opening of the vestibule is the primary aim of all operations for 
suppurative labyrinthitis. Jansen opens the vestibule above and behind, 
and believes it unnecessary, unless its margins are necrotic, to enlarge the 
oval window downward or to remove the outer wall of the promontory. 
In this belief he is at variance with all other surgeons who have jnade 
suppurative labyrinthitis a special study. Hinsberg and Neumann appar¬ 
ently believe that by opening the vestibule freely above, and then removing 
the outer wall of the promontory, we secure drainage both of the vesti¬ 
bule and the cochlea, and that this in the great majority of cases fulfils 
every surgical indication. The operation proposed by Richards calls for 
separate exposure of each semicircular canal, free opening of the vestibule, 
removal of the outer wall of the promontory, and, when the cochlea is 
apparently extensively involved, for complete uncovering of the infected 
cochlear spaces. We shall return later to a discussion and analysis of 
these somewhat divergent views. 

Surgical Guides to the Vestibule.—The following structures may be 
utilized as surgical guides to the position of the vestibule: 


THE JANSEN OPERATION 


465 


(a) The anterior, or ampullar, end of the horizontal semicircular canal: 
Removing the upper wall of this part of the canal,— i.e., uncovering it 
superiorly,—the roof of the vestibule lies just behind, or rather internal 
to, its ampulla. 

(b) The posterior end of the horizontal semicircular canal: This may 
with care be traced to its small opening in the posterior wall of the vestibule. 

(c) The so-called “ solid angle”: By opening separately the three semi¬ 
circular canals, and observing the point at which their respective planes 
intersect one another, we are able to deduce the position of the vestibule. 

(d) Combined use of oval window and ampullar end of horizontal canal: 
The oval window having been enlarged by removal of the promontory a mi¬ 
nute probe, the end of which is bent to a right angle, is introduced through 
the oval window and carried upward to the vestibular roof, which lies be¬ 
hind the ampullar end of the horizontal canal (Hinsberg). 

(e) Approaching the vestibule from the posterior fossa (Neumann), 
the posterior vertical and the horizontal canals are opened; the line in which 
their planes intersect each other leads directly to the vestibule. 

Operation. —Whatever operative method is adopted, the opening of 
the labyrinth must be preceded by a very complete radical operation. If 
the position of the sigmoid sinus permits, the antromastoid cavity should 
be enlarged backward sufficiently to allow ample room for the manipula¬ 
tion of instruments. The “facial spur” should be reduced to the lower 
limit of safety and always sufficiently to bring the stapes or oval window 
into clear view. Other structures which should be clearly seen are the niche 
of the round window, the horizontal portion of the facial canal, and the 
prominence of the anterior half of the horizontal canal. These represent 
preliminary steps in any operation for diffuse suppurative labyrinthitis. 
It should be said here that for the operation upon the labyrinth itself 
brilliant illumination, either by reflected light or, better, by the electric 
forehead lamp, is absolutely essential. 

The Jansen Operation (intratympanic).—Jansen begins by remov¬ 
ing the roof of the horizontal semicircular canal. In accomplishing this 
great care is observed not entirely to obliterate the canal or to injure its 
floor, since the removal of too much bone in this direction endangers the 
integrity of the facial canal which lies just beneath. Having uncovered 
the canal by removal of its superior wall, its anterior end and ampulla are 
used as guides to the lower limit of safety,— i.e., below which the facial 
canal is likely to be fractured. The posterior portion of the horizontal 
canal, which curves backward and away from immediate proximity to the 
Fallopian aqueduct, he removes wholly. He now has a choice of two 
points of attack at which to open the vestibule,—viz.: (A) Anteriorly,— 
i.e., to the inner, or medial, side of the ampullar end of the horizontal canal. 
By this route, which perforates the tympanic roof, great care is necessary 
to avoid fracturing the ridge of bone which includes both the floor of the 
horizontal canal and the horizontal portion of the facial canal. (B) The 
vestibule may also be reached posteriorly,— i.e., by tracing the horizontal 
30 


46G TREATMENT OF SUPPURATIVE LABYRINTHITIS 


canal in the direction away from its ampulla, and finally excavating in 
the direction of its small end, which opens upon the posterior wall of the 
vestibule. The latter course is regarded as providing greater security to 
the facial nerve. Having entered the vestibule by the posterior route, 
the opening is enlarged by the careful removal of the roof, i.e., parallel 
with the anterior arm of the horizontal canal and in the direction of its 
ampulla. This provides a free opening of the vestibule through its pos¬ 
terior wall and roof, and usually completes the operation. 

If its margin shows no evidences of necrosis, the oval window is not 
enlarged downward and the outer wall of the promontory is not removed. 

Hinsberg’s Operation. —The preliminary radical operation having 
been completed, Hinsberg recommends beginning the labyrinthine opera¬ 
tion by enlarging the oval window. The stapes if present is extracted. 
The enlargement of the oval window is commenced by removal of the 
small bridge of bone connectiong the oval and round windows. With 
a small curette, the window is now further enlarged by removal of the outer 
shell of the promontory forward and downward. A small tympanic probe 
with the end bent to a right angle is now introduced directly through the 
enlarged oval window and carried upward to the roof of the vestibule. 



Groove representing 
floor of horizontal 
canal , probe emerg¬ 
ing through un¬ 
covered vestibule 

Bridge containing 
facial nerve and floor 
of horizontal 
semicircular canal 


Cochlea opened by 
partial removal of 
outer wall of 
promontory 


Fig. 270.—Hinsberg’s labyrinthine operation. 


This indicates the position and level of the roof of the vestibule. We must 
now remove the roof of the ampullar end of the horizontal canal, which 
requires the reduction of its co-called “prominence” from above down¬ 
ward until its lumen is exposed. This may be accomplished by shaving 
off thin layers of bone with a small straight-edged chisel, by means of a 
curette, or by the careful use of an electric burr. When the lumen of the 
canal is exposed, the tympanic probe may again be introduced. The roof 
of the vestibule, having been thus definitely located by its relation to the 
ampulla of the horizontal semicircular canal and by the direction of the 







HINSBERG’S OPERATION: RICHARDS’S OPERATION 467 


probe, is perforated by means of a burr or very small chisel. The opening 
is then enlarged backward (Fig. 270). 

To summarize: The successive steps of the Hinsberg operation are 
(a) enlargement downward of the oval window and removal of the outer 
wall of the promontory; this exposes freely the lower part of the vestibule 
and the basal whorl of the cochlea; (b) removal of the superior wall of the 
ampullar end of the horizontal semicircular canal; (c) perforating the roof 
of the vestibule and subsequent enlargement of this opening; (d) removal 
by very careful curettage of diseased structures— i.e., granulations, etc.— 
from the spaces so exposed. In the author’s opinion, this is a rational, 
safe, and fairly complete method of draining the vestibule. 

Richards’s Operation. —This method proposes the separate exposure 
and opening of each of the three semicircular canals. When this has been 
accomplished, we have clearly indicated the planes of the three canals 
which stand at right angles to each other and enclose what is spoken of as 
“the solid angle.” The roof of the vestibule falls within the plane of the 
horizontal canal. By the solid angle is presumably meant the angle formed 
at the point where the respective planes of the three canals intersect each 
other (Fig. 271). This marks the point beneath which the common tube 

Anterior vertical semicircular canal 


(d) solid angle 


vertical 

canal 

Fig. 271. —So-called “solid angle.” 

of the two vertical canals bends outward to enter the vestibule. It is at 
this point that Richards enters the vestibule, creating here a conical 
depression which is gradually lowered until the vestibule is reached. “The 
opening of the vestibule is now enlarged until a full exposure is obtained of 
this portion of the cavity.” The remainder of the operation includes the 










468 TREATMENT OF SUPPURATIVE LABYRINTHITIS 


removal of the bridge of bone connecting the oval and round windows and 
the uncovering of the first cochleal whorl by removal of the outer shell of 
the promontory from behind forward and downward. In cases in which 
the cochlea has been extensively invaded, Richards advises that it be 
exposed and opened to the extreme limit of the morbid process. 

Neumann’s Operation approaches the vestibule from the posterior 
fossa of the skull. 

Preliminary Steps .—The radical operation is completed in the usual 
way, and the sigmoid sinus is in part uncovered. In front of the anterior 
margin of the sinus, the bone covering the cerebellar dura is removed from 
the tegmen antri above to the forward bend of the sinus below. The dural 
covering of the cerebellum is thus exposed over a triangular space which is 
bounded above by the roof of the mastoid, behind by the sigmoid sinus, 
and in front by the base, or posterior surface, of the petrous pyramid. 
This posterior surface of the os petrosa constitutes the operative field from 
which a pathway to the labyrinth is made. 

The Labyrinthine Operation .—The vestibule is approached by the 
gradual cutting away of the posterior surface of the petrous bone. This is 
best accomplished by means of a sharp chisel or gouge. As successive very 



Fig. 272.—Vertical section through aditus and vertical portion of facial canal. 


thin layers of bone are removed, the bone surface should be scrutinized for 
the first exposure of the posterior vertical semicircular canal. This may 
first be recognized as a short linear discoloration or, if its lumen is opened, 
as a short vertical tunnel representing the open canal. As the removal of 
bone proceeds, this part of the posterior vertical canal is also removed. 


NEUMANN’S OPERATION 


469 


Above and below, however, are seen two small circular orifices which repre¬ 
sent cross-sections of the canal, from which points its superior and inferior 
arms are continued to their termination in the vestibule. Further removal 
of bone brings next into view the posterior arc of the horizontal semicircu¬ 
lar canal, its lumen lying horizontally and at right angles to the plane of 
the posterior vertical. When this also has been cut away, we see a third 
small circular orifice in the bone, lying about midway between and a little 
external to those first noted. This, of course, represents a cross-section of 
the posterior arm of the horizontal canal, which terminates in the posterior 
wall of the vestibule (Fig. 272). 

If we imagine lines joining the three orifices so exposed, we have en¬ 
closed a slender triangular space, the centre of which will mark the point 
of our attack upon the vestibule (Fig. 273). Having thus determined the 



Fig. 273. —Surgical guides to vestibule (Neumann’s operation). 

point of attack, we have three sources of information as to the direction 
which the excavation shall take to perforate the posterior wall of the ves¬ 
tibule,—viz., (a) its known relation to tympanic landmarks,— e.g., its 
position just behind and chiefly above the oval window; (b) the obvious 
direction of the open posterior crus of the horizontal canal; and (c) the 
estimated plane of the posterior vertical canal, the two ends of which we 
have open before us. This avenue of approach has the advantage of being 
well behind the bend and descending portion of the facial canal, so that 
the facial nerve is in no danger of injury at this stage of the operation. 

The vestibule having been exposed through its posterior wall, the 
opening may be enlarged by the careful removal of the roof. The removal 







470 TREATMENT OF SUPPURATIVE LABYRINTHITIS 


of the promontory from the oval window downward and forward is carried 
out in the usual manner. 

Comparative Advantages and Disadvantages of the Different 
Operations. — Jansen’s operation is a practical method of uncovering 
the upper portion of the labyrinthine vestibule. As a therapeutic measure 
its efficacy is marred by its failure to provide drainage below by the en¬ 
largement of the oval window and the removal of the outer wall of the 
promontory. To this is probably due the unusually large percentage of 
deaths (25 per cent.) in Jansen’s recorded series of labyrinthine operations. 

Hinsberg’s operation provides a systematic and comparatively safe 
method of opening the vestibule and basal turn of the cochlea which, if 
properly executed, can not fail adequately to drain these spaces. As 
compared with the Neumann operation, it offers a distinct advantage, 
in cases in which the disease is confined within the labyrinth, in that the 
sigmoid sinus and dural covering of the cerebellum are not uncovered. In 
execution it is simpler than Richards’s operation and the surgical guides 
utilized in locating the vestibule are more definitely indicative of the 
position of that little cavity. 

Richards’s operation differs in its mechanical results from those of 
Jansen and Hinsberg in its insistence on the separate opening of each 
semicircular canal and the complete exploration of the cochlea when the 
cochlea is extensively involved. As described by its sponsor, it presents 
the following difficulties for the student,—viz.: (a) no directions are given 
for locating the two vertical canals, and their delineation is essential to 
the utilization of the so-called “solid angle;” and (b) the term “solid 
angle” is a somewhat indefinite expression which conveys no impression 
of the exact point for opening the vestibule. 

Neumann’s operation offers the following advantages over the others: 
(a) The risk of injury to the facial nerve is practically or almost nil; (b) 
in case of suspected deep-seated epidural abscess in the cerebellar fossa, 
this lesion is investigated and perhaps relieved by this operation; and, 
again, such lesions, though unsuspected, are sometimes brought to light 
by this method; (c) Neumann claims that the formation of healthy granu¬ 
lations occurs more rapidly from healthy dura than from the dense bone 
of the labyrinth, and that the period of postoperative healing is, therefore, 
actually shorter than by other methods. 

The chief objection to the Neumann operation is the unwillingness of 
many surgeons to open the brain cavity in the absence of suspected intra¬ 
cranial disease, and the risk, however small, which such exposure entails. 
When the sigmoid sinus is placed far forward,— i.e., very near the pos¬ 
terior wall of the bony meatus,—Neumann’s operation is not practicable. 

Before leaving the discussion of operative methods or technic, the writer 
wishes to describe very briefly a method of opening the vestibule which 
has seemed to possess the advantages of simplicity and comparative safety. 

Author’s Method of Reaching the Vestibule. —The preliminary 
radical operation prepares as usual the way for the surgical attack upon 


TECHNIC OF OPENING THE VESTIBULE 


471 


the labyrinth. This leaves in view the tympanic landmarks, including the 
prominence of the horizontal semicircular canal (Fig. 274, a). Above this 
prominence, and between it and the tegmen tympani, is a space usually 
containing more or less diploic tissue (Fig. 274, 6). The first step toward 



Fig. 274.—Radical operation preliminary to opening labyrinth. 


the vestibule is made by thoroughly excavating this space by means of a 
suitable bone curette. This leaves an open space of variable height and 
considerable depth above the horizontal canal and vestibule (Fig. 275, a). 
The next step is the exposure of the lumen of the horizontal canal by re¬ 
moval of its upper wall. If we attempt to accomplish this by means of a 
chisel,—even though we try to remove only the thinnest layers,—we run a 
very considerable risk of causing a fracture involving the facial canal, with 
resulting facial nerve injury. If we employ the ordinary curette, the force or 
pressure required in its use involves a similar danger. The writer believes 
that he eliminates these risks very largely by the use of a specially designed 
curette (Fig. 276), the edges of which are very sharp. In employing this in¬ 
strument, one should depend upon the sharpness of its cutting edges and use 
rather rapid scraping movements, with relatively little pressure, to lower or 
excavate the bone from above downward. In this way the upper surface of 
the bony shelf containing the horizontal canal and covering the vestibule is 
rapidly scraped away. Sufficient force is not used to risk fracturing the bone. 
While this excavation is in progress, the upper bone surface is under 
constant scrutiny for the first signs of the horizontal semicircular canal. 
This is first seen as a linear discoloration, or rather loss of ivory-whiteness 
under the bone surface, and then, as its lumen is opened, as a very narrow 











4?2 TREATMENT OF SUPPURATIVE LABYRINTHITIS 


linear depression. This method of uncovering the canal has the advantage 
of absolute safety so far as any risk of producing a fracture into the facial 
canal is concerned. As soon as the canal is opened, it should be traced 



Fig. 275. — Excavation preliminary to un¬ 
covering vestibule. 



Fig. 277.—Vestibule with roof removed. 



Fig. 276.— 
Author’s cu¬ 
rette. 


forward by means of the same instrument to the beginning of its ampulla, 
and backward to the beginning of its posterior arc. This gives the physical 
condition shown in Fig. 277, o. In exposing the canal by this method, we 








































TECHNIC OF OPENING THE VESTIBULE 


473 


are simultaneously reducing the thickness of the bone constituting the 
roof of the vestibule, and thus rendering easier the next step of the opera¬ 
tion,—viz., the actual exposure, or opening, of the vestibule. We locate 
the roof of the vestibule bv its known position just behind, or internal to, 
the ampulla of the horizontal canal, and also its position internal to a 
vertical line passing through the niche of the oval window. By elevating 
the handle of our special curette we may now excavate the space behind 
the anterior end, or ampulla, of the horizontal canal and quickly enter 
the vestibule. In doing this we should avoid too great haste, as by exert¬ 
ing excessive pressure at this point we may place too great a strain upon 
the ridge of bone containing the horizontal and facial canals, and cause its 
fracture. Once the vestibule has been uncovered, it is an easy matter to 
enlarge the opening backward to the point, if desired, of completely re¬ 
moving the posterior arc of the horizontal canal. This, however, I believe, 
is rarely called for, and I can not see that it serves any particularly useful 
purpose unless we have physical evidences of an extension of necrosis in 
this direction. 

If the stapes has been removed, we may now pass a small bent tympanic 
probe through the oval window and upward into our opened vestibular 
cavity, or vice versa (Fig. 277, b). The oval window is next enlarged and 
the promontory removed by methods already indicated. 

The operation for diffuse suppurative labyrinthitis is admittedly a diffi¬ 
cult one; but for the student its inherent difficulties have been both magni¬ 
fied and multiplied in some of the descriptions of technic which have been 

written. 

Having outlined and compared the various surgical pathways to the 
labyrinth, it may be well to return briefly to a discussion of certain prob¬ 
lems involved in labyrinthine surgery, whatever operative method be 

adopted. 

In addition to the facial nerve, four structures or regions are said to be 
in some danger of injury during a labyrinthine operation,—viz., the bulb 
of the jugular vein, the carotid artery, the internal auditory meatus, and 

the modiolus. 

The jugular bulb and carotid artery may be dismissed with a word. 
They are at no risk in the hands of a careful surgeon. Even when abnor¬ 
mally placed,—the jugular bulb projecting high into the hypotympanum 
or the artery being exposed through a dehiscence in the carotid canal, * 
they should be safeguarded by the deliberate care which should attend 
every step of an operation upon the labyrinth. I can think of but one 
source of danger to these vessels in such an operation—viz., the use of an 
electric burr. One can readily imagine that, with eithei vessel occupying 
an abnormal position, this instrument might easily enter it before the 
surgeon could discover its malposition. This fact might find expression 
in a surgical rule,—viz., that the electric burr should not be used in the removal 

of the promontory. . .. , , ,, 

Internal Auditory Meatus. —The dura here is firmly adherent to the 


474 TREATMENT OF SUPPURATIVE LABYRINTHITIS 


subjacent bone and is, therefore, peculiarly subject to injury. The point 
of a chisel entering the meatus either from the cavity of the vestibule or 
region of the base of the modiolus would, therefore, almost inevitably 
produce rupture of its dural lining. According to Richards, accidental 
opening of the internal meatus is likely to be followed by rapid and serious 
loss of cerebrospinal fluid, and places the patient in great danger of menin¬ 
geal infection. The loss of cerebrospinal fluid apparently occurs only 
when the dural lining of the meatus is ruptured. I know of two cases—• 
one of which came in my own surgical experience—in which the internal 
meatus was opened with a curette. In neither of them was there any 
noticeable loss of cerebral fluid. For this reason, I am inclined to believe 
that the chisel is an exceedingly dangerous instrument for use in the neigh¬ 
borhood of the internal meatus. I myself in the case referred to above 
opened the internal meatus with a curette, with no loss of cerebrospinal 
fluid and no meningeal symptoms. I agree with Richards, however, that 
opening of the internal meatus should be carefully avoided. 

Modiolus .—There seems to be little question that the structure injury 
of which entails greatest risks is the modiolus. That we cannot make a 

thorough surgical exploration or exposure of the 
cochlea without removing some portion of the 
modiolus is made perfectly clear to us when we 
look at a section through the cochlea from base 
to apex (Fig. 278). If the modiolus has been 
actually destroyed by disease, it is possible that' 
its channels have been closed by the inflamma¬ 
tory process in advance of the necrosis. If such 
destruction has not occurred we shall do well to 
content ourselves with providing free drainage 
from the vestibule and first cochlear turn, and 
not attempt such radical exposure of the cochlea 
as will throw open the innumerable little channels within the modiolus. 
In other words, I believe that in operating upon the labyrinth, we deal 
properly with the modiolus when we leave it as nearly as possible alone. 

In support of the above dogma we should bear in mind the chief purpose 
of the labyrinth operation, which is primarily to save life by preventing a 
spread of the infection to brain or meninges. Of the natural channels by 
which pus from the labyrinth may reach the intracranial cavity, those 
traversing the modiolus oftenest lead to intracranial disease. When we 
remove any part of the modiolus, we shorten and open wide these most 
dangerous pathways, and assume a risk altogether disproportionate to any 
advantage which may be expected from our misplaced surgical zeal. 

This brings us to the question,—is drainage all that the labyrinthine 
operation should aim to accomplish? Personally, I believe that in the 
great majority of cases it is. The interior of the labyrinth differs from 
extra-labyrinthine parts of the temporal bone in this important particular, 
—viz., it contains no diploic or pneumatic structures, its walls being every- 



Fig. 


278. — Horizontal section 
through cochlea. 



LAKE’S OPERATION FOR RELIEF OF VERTIGO 


475 


where formed of hard, dense bone. Thorough drainage should therefore, 
place the labyrinthine spaces under very favorable conditions for rapid 
resolution. Even though the cochlea be extensively involved, it is surely 
safer to depend upon such drainage as is provided by removal of the 
promontory than to extend our exploration at the risk of opening + he 
numerous channels within the modiolus, and thus facilitate the passage of 
infective matter to the meninges through what is admittedly the most 
dangerous pathway from the labyrinth. 

I agree with Jansen that it is not necessary to open and exploie sepa¬ 
rately each semicircular canal. When a fistula leads into one of the canals, 
the necrotic tract should, of course, be eliminated. But the walls of the 
bony canals are formed of very hard, dense bone, rarely becoming necrotic 
from within. The canals open only into the vestibule, and when the ves¬ 
tibule has been freely opened, adequate drainage of the canals has also 
been provided. That these conclusions are in accord with clinical results 
is supported by the fact that Hinsberg’s operation, which insists only upon 
the opening of a single canal,— 1 . 6 ., the horizontal, has in the seivice of 
the University Hospital of Breslau yielded a mortality of only 4 per cent. 

In conclusion, the writer wishes to reiterate his belief that the latent 
stage of suppurative labyrinthitis is that during which the labyiinth can 
be operated upon with least risk to the patient. If, therefore, we can 
bring our patient through the acute stage of the disease without operative 
intervention, we may then operate with greatly increased chances of a 
successful issue. It is probably in appreciation of this ratio of the danger 
to the stage of the disease that Heine recommends that granulations be 
scraped from a labyrinthine fistula only if the symptoms of vestibular 
irritation have completely disappeared. In support of this contention he 
cites a case reported by Jansen in which "granulations were scraped out 
of a labyrinth which had been opened the week before, with the result 
that the'patient developed meningitis and died.” Carrying the idea still 
further, it would seem safer, in cases of suppurative invasion of the laby¬ 
rinth following surgical injury at the oval window, to content oneself with 
simple drainage;— i.e., having uncovered the _ vestibule above and the 
first cochleal whorl below, any curettage within these spaces should )e 
studiously avoided as likely to determine the passage of infective matter to 
the meninges This, of course, is m accord with the belief that when the 
latent stage is reached, the pathways of infection are to some extent closed. 

Obliteration of the Vestibule for the Relief of Vertigo (Lake). Be¬ 
fore leaving the subject of labyrinthine surgery, a word should be said 
of the pioneer work of Mr. Richard Lake in obliterating the membranous 
vestibule in cases of intractable and unbearable vestibule.' vertigo not 
dependent upon suppurative labyrinthitis. While successful operations 
for to purpose had previously been performed by Milligan,’ his opera- 


■ Lake: Operation on the Vestibule for the Relief of Vertigo, Lancet, Jan. 6 , 1906. 
2 Milligan: cited by Lake, ibid. 







476 TREATMENT OF SUPPURATIVE LABYRINTHITIS 


tions had consisted of the removal of the prominent external arc of the 
horizontal semicircular canal. We now know that, if we essay to annul 
the function and irritability of the vestibular nerve, it is more logical to 
destroy completely the structures of the membranous labyrinth, and far 
safer to open fully the labyrinthine vestibule than to open a single semi¬ 
circular canal; for the slighter operation, to be successful, must lead to 
ablation of function of the entire vestibular mechanism, and it may equally 
as well lead to diffuse suppurative labyrinthitis should the postoperative 
wound by any chance become infected. 

Lake’s operation consists of the removal of the roof of the external 
semicircular canal, the tracing of this canal to its terminal openings into 
the vestibule, thorough removal of the roof of the vestibule, and the pro¬ 
vision of a counter opening below the horizontal portion of the facial 
canal by extraction of the stapes. 

This procedure, as also in some cases was the technically simpler opera¬ 
tion of Milligan, has proved successful in attaining the chief end in view, 
—viz., the relief of the vertigo. The operation, while it has proved suc¬ 
cessful in Lake’s hands, is indicated only in a very limited class of cases. 
Mr. Lake himself states that it should not be employed in the case of 
individuals with good hearing power, or even for those with a useful 
residue of hearing. In other words, he regards his operation as indicated 
only in cases in which the cochlear function is so far lost as to render its 
preservation a negligible consideration. Whatever degree of hearing the 
patient majr possess, absolute deafness in the ear operated upon is the 
inevitable outcome of this operation. 


CHAPTER XVII. 

SURGICAL TREATMENT OF INFECTIVE SIGMOID SINUS THROMBOSIS. 

Before entering upon a description of operative methods, it may be 
well to refer briefly to certain questions which bear directly upon the 
treatment of sinus disease, and which are yet open to discussion. 

Until quite recently it was almost an axiom among the leading aurists 
of America that, when a suppurative lesion within the sigmoid sinus 
demands that this vessel be isolated from the general blood stream, the 
jugular vein should be exposed and resected from a point a little above 
the clavicle to a point above the entrance of the facial vein. 

As opposing this view must be considered the interesting and remark¬ 
ably successful series of cases reported a few years since by Dr. Crockett, 
and to which reference has already been made. In these cases, sixty in 
number, and operated upon by the various surgeons of the Boston Eye 
and Ear Infirmary, the vein was simply divided between two ligatures, no 
part of it being removed. Including within this series certain cases in 
which evidences of meningeal or brain lesion were present before the 
operation, the mortality was 16 per cent. By excluding the cases of pre¬ 
existing brain or meningeal involvement, the mortality is reduced to 9 
per cent. These results are at least as good as any following jugular resec¬ 
tion of which I have seen reports. 

When in Vienna four years ago, the writer was shown several cases of 
sinus thrombosis in the hospital wards presided over by the surgeons of 
the Politzer-Urbantschitsch Clinic, which had been operated upon by 
simple ligation. He was told that ligation was the method there employed 
in cases not giving physical signs of extensive jugular thrombosis, and that 
the results were regarded as satisfactory. Returning to Vienna two years 
later, he learned that these views had not been modified. 

Dr. J. J. Thompson, of New York, recently told the writer that he 
had in the past few years followed the Boston school in operating upon a 
number of cases of infective sinus thrombosis by simple ligation, the liga¬ 
ture being applied in many cases below the entrance of the facial, and that 
the results were quite as good as any he had observed from jugular resec¬ 
tion. In a case recently operated upon by the writer, the patient’s con¬ 
dition was so unfavorable that doubt was expressed as to whether he would 
survive an operation. The operation had progressed as far as the exposure 
of the lower end of the jugular when the patient showed signs of collapse, 
and the operation was ended abruptly by the resection of a small portion 
of the vein considerably below the entrance of the facial. In this case 
the resected portion was so small and so situated as to be equivalent 
in effect to a ligation. The patient made a fairly rapid recovery. 

The above facts are at least sufficiently impressive to justify me in 
urging that we hold this question open to discussion and oui minds recep¬ 
tive to further evidence. 


477 


478 SURGICAL TREATMENT OF SINUS THROMBOSIS 


The arguments in favor of resection as opposed to simple ligation of 
the jugular are based upon the fact that the intima is often found to be 
extensively diseased over a considerable portion of its entire length, in 
which case resection would seem the only adequate treatment. The re¬ 
moval of the vein to a point above the entrance of the facial is insisted 
upon as a means of preventing a reversal of the blood stream and dissem¬ 
ination of septic matter through the latter vessel. Upon theoretic grounds 
this operation seems both logical and thorough, and the results have as 
a whole been regarded as satisfactory. 

The advantages claimed for simple ligation of the jugular vein as 
compared with resection are (1) its comparative simplicity; (2) the usual 
absence of shock; (3) absence of disfiguring postoperative deformity or 
scar; and, finally, its advocates claim that, through the smaller drain 
upon the patient’s vitality and nervous force, the results are better. 

Personally the writer has so far followed the practice in vogue among 
his hospital associates, and, with the single exception of the case above 
cited, has resected the vein from a point somewhat above the clavicle to a 
point above the entrance of the facial. While he has had under his care 
a large number of cases in which the outer sinus wall was extensively 
diseased and of others presenting symptoms strongly suggestive of sinus 
thrombosis, his actual operative experience has been comparatively small. 
He has resected the jugular vein in 14 cases, of which 4 died and 10recovered. 
Three of the fatal cases were secondary to severe systemic disease, one diph¬ 
theritic and two complicating scarlet fever of severe type. 

In the above statement I have tried to present impartially the two 
sides of this question as one still sub judice. As to my personal belief, a 
review of the subject has forced me to the conclusion that in a majority of 
the cases in which the jugular vein has been resected, most of my own 
cases being included, the simpler operation of ligation would have fulfilled 
the surgical indications quite as well, with less disfigurement in the result¬ 
ing scar and with less danger to the patient in the considerable shock 
which occasionally results from jugular resection. 

As to the question of whether there is any class of cases in which ligation 
may be distinctly preferable, it seems to the writer that a positive indica¬ 
tion for the simpler operation may be found in cases of great systemic 
exhaustion in which every minute saved from the anaesthetic and operative 
strain adds to the patient’s chances of recovery. 

Before considering the operative treatment in detail, I wish also to say 
a word in regard to a question upon which otological literature throws 
little light, viz., in what class of cases is the sinus operation alone— i.e., 
without jugular ligation or resection—indicated? Theoretically this ques¬ 
tion is easily answered by the statement that it is indicated* in cases in 
which the physical evidences on opening the sinus are of a circumscribed 
lesion situated well above the lower end of the vertical limb. But how are 
we to determine such limitation? Suppose, for example, that we operate 
upon a case in which symptoms of periodic septic absorption have been 
present, and that on opening the sinus we have free bleeding from the 


TECHNIC OF SINUS OPERATION 


479 


direction of the bulb, and a demonstrable clot toward the torcular end. 
Such a case would seem to present ideal conditions for the sinus operation 
alone. But can we be sure either that a secondary infection at the bulb 
does not already exist, or that in the manipulation incident to the opening 
of the sinus, its compression below and the removal of a septic clot above, 
we have not sown the seed for septic thrombosis below? Or suppose that 
we find absolutely no physical evidences of a clot; can we from this con¬ 
clude that a non-obstructive parietal clot does not exist in the bulb? 
Personally I feel that when we have opened the sinus to the extent neces¬ 
sary to explore its lumen for the presence of a suspected clot, we have 
incurred the risk of producing a traumatic thrombus even though none 
has previously existed. For this reason and those stated above, I believe 
that, when we have assumed the responsibility of opening a sinus on account 
of symptoms of septic absorption, we should in every case further safe¬ 
guard the patient by ligation or resection of the jugular vein. 

As to which operation should precede the other,— i.e., the exploration of 
the sinus or the ligation or resection of the vein,—two views are held,—viz.: 

I. That the sinus should he explored first, because (a) to tie the jugular 
vein in advance of the sinus operation might cause a reversal of the blood 
current in the sigmoid and lateral sinuses, and thus carry infective matter 
from a septic thrombosis in the sigmoid to the venous channels of the 
opposite side, or through the superior petrosal to the cavernous sinus, etc.; 
and (b) in case of a disintegrating clot within the bulb, the ligation of the 
vein before the current is checked from above may so increase the pressure 
upon the clot as to force infective matter into the collateral vessels out¬ 
side of the skull,— i.e., those communicating with the upper end of the 
vein,—and thus establish new foci of infection. These contentions, while 
theoretically correct, are not in my opinion of great practical significance. 

II. That the jugular vein should he ligated or resected before the sums is 
opened, for the reason that, if the reverse order is observed, the manipula¬ 
tion of the sinus, and particularly the use of compresses, may dislodge and 
force into the general circulation portions of an infected clot which other¬ 
wise might be removed through the sinus wound. 

Ordinarily, I do not believe that it greatly matters which operation is 
performed first. When, however, the patient’s condition is so profoundly 
septic and his vitality so greatly reduced that the addition of any fresh 
septic material to that already circulating in the blood might turn the scale 
unfavorably, I should say that ligation of the vein should precede the 
opening of the sinus. 

In any case, and whichever order of precedence is observed, the sinus 
should always be freely exposed and ready for exploration before the vein 
is operated upon. 

Sinus Operation for the Removal of an Infected Clot.—In describ¬ 
ing this operation, we shall assume that a very complete preliminary 
mastoidectomy has been performed. In mastoid surgery it is a technical 
rule that the margins of the bony wound should, as far as may be, present 
shelving surfaces,— i.e., its posterior boundary should not present a sharp 


480 SURGICAL TREATMENT OF SINUS THROMBOSIS 


edge of cortex leading precipitately into a deep cup-shaped cavity. When 
the sinus is to be exposed, it is particularly important that the cortex 
should be freely removed behind the sinus groove, since the attempt to un¬ 
cover the sinus at the depth of a narrow bony depression would be both diffi¬ 
cult and dangerous. Obviously, it would be neither easy nor safe to attempt 
the exposure of the sinus until its bony groove had been clearly outlined 
throughout the greater extent of the mastoid cavity. This usually, though 
not invariably, delineates the vessel’s course from the knee, or bend, above to 
the point at which it curves forward below to enter the jugular foramen. 
The preliminary mastoid operation, properly executed, should leave a bony 
cavity, or excavation, somewhat resembling that shown in Fig. 279. 

For the initial removal of bone from the intact sinus groove, a flat 
chisel of moderate width is undoubtedly the safest instrument. Usually 
it is more convenient to remove the first layer of bone from behind forward 
rather than vertically,— i.e., along the course of the sinus. The chisel 



Fig. 279. —Bone operation preliminary to exposure Fig. 280. —Position of chisel in uncovering the 
of sigmoid sinus. sigmoid sinus. 


should be held as slantingly as possible,— i.e., with its flat surface lying as 
nearly flat upon the surface of the sinus groove as will allow its edge to 
engage the bone (Fig. 280). Only the slightest taps of the mallet should be 
used. Employed in this way the chisel penetrates the bony plate of the 
sinus groove, but practically never injures the dural coat of the vessel, 
unless the latter is actually adherent to the overlying bone. The latter 
condition is usually indicated, however, by the macroscopic appearance 
of the bone, and will be further indicated by its softness and the ease with 
which the chisel enters the bone. When the edge of the chisel has passed 
beneath the sinus plate for a little distance, it is withdrawn slightly and 
then, by cautiously lowering the handle, the first scale of bone is gently 
prized upward and removed, exposing the dura beneath. By repetition of 
this process—using always the greatest care—the first exposure of the sinus 
is gradually enlarged. When we have uncovered the sinus over an area 
approximately half an inch in length and of sufficient width to admit of 
the introduction of instruments beneath the bone, it is usually safer and 
easier to lay the chisel aside and substitute other instruments. If now we 







TECHNIC OF UNCOVERING SINUS 


4S1 


can introduce a curved round-edged separator between the sinus and the 
overlying bony plate, showing absence of adhesions, we are in a position 
to use some form of rongeur with advantage. 



Fiq. 281.—Rongeur. 


Fig. 282.—Rongeur. 


Use of the Rongeur. —For uncovering the sinus the rongeur is either 
a safe or a very dangerous instrument according to the type of instrument 
and the way it is used. A sharp, thin-bladed rongeur (Fig. 281) is a dan¬ 
gerous instrument for this particular work, on account of the ease with 
which its edge may engage a hidden dural surface. Fig. 282 shows a 
31 
















482 SURGICAL TREATMENT OF SINUS THROMBOSIS 


rongeur the thick, rounded cutting extremity of which may be actually 
employed to separate the sinus wall from its bony covering. As to the 
method of using the rongeur for exposing the sinus, if one blade is made to 
engage the edge, or margin, of the bony opening, and the other is made to 
engage the cortex further back, this cortical point being used as a fulcrum, 
the exposure may be quickly enlarged, but there is always danger that the 
lower blade may slip slightly and the sinus wall be caught between its 
edge and the bone to be removed. A much safer method is by using the 
comparatively thick-bladed rongeur (Fig. 282), the lower blade of which 
is introduced between the sinus wall and overlying bone, and made to do 
actual duty in separating the one from the other. By slightly withdrawing 
the instrument just before the blades are brought together, there is little 
danger of opening the sinus. 

The objection which has been advanced to the use of the rongeur,— 
viz., that the introduction of any instrument between the bone and sinus 
wall may by its displacement of the latter dislodge a parietal clot,—is, of 
course, theoretically tenable. It is, however, a purely theoretic contention, 
since such an accident is not known ever to have occurred, nor does it seem 
mechanically probable. 

The sinus should be exposed from the knee to the lowest point before 
it bends forward to disappear within the jugular bulb (Fig. 283).' 

The various macroscopic changes occasionally observed in the outer 
sinus wall have been described in a foregoing chapter, and need not be 

dealt with here. The sinus has been 
found to contain a septic clot in cases 
in which the outer dural coat was of 
normal appearance; and, per contra , 
it is not uncommon to see the outer 
coat covered with granulations or 
showing other pathologic changes 
while the interior of the vessel remains 
quite free of disease. We are not, 
therefore, able to determine from the 
physical signs alone the presence or 
absence of an infective clot within the 
sinus. 

In preparation for the opening of 
the sinus, the entire wound should be 
flushed out with sterile normal salt solution. Fresh sterile towels are 
placed about the head and around the wound. The surgeon's hands 
are re-sterilized, or, if operating in gloves, these are changed. All 
instruments used in the preliminary operation are discarded or re¬ 
sterilized,— i.e., only freshly sterilized instruments should be used for the 
intra-sinous operation. 

The instruments especially needed for exploring the sinus are an ordi¬ 
nary scalpel (kept in alcohol until needed), flat scissors and scissors curved 



Fig. 283.—Exposure of sinus wall preliminary to 
its exploration. 



EXPLORATION OF SINUS 


483 


on the flat, both sharp, two ordinary thumb forceps for holding iodoform 
plugs, bayonet forceps, toothed forceps, and one or two dull ring curettes. 
There must also be in readiness a number of gauze plugs—for safety, say 
a dozen—consisting of small, tightly rolled bundles of iodoform gauze, 
about three-eighths inch in length and of the diameter of a small lead-pencil. 
These are very essential for the control of hemorrhage (see Fig. 235). 

In addition to the above, there must also be at hand mallet and chisels 
or rongeurs, scalpels, periosteal elevators, artery-clamps, etc., for use in 
case the conditions within the sinus should call for further removal of bone, 
— e.g., for the exposure of the lateral sinus from the sigmoid bend back¬ 
ward toward the torcular. 

Exploration of the Sinus. —In this operation our aim is to expose 
the interior of the vessel to actual inspection. To attempt less but adds 
to the patient’s risks, and supplies the surgeon with absolutely no data of 
diagnostic value. It is not sufficient, therefore, to puncture the vessel, or 
even to make a short incision in its outer wall over that region in which we 
believe infection most likely to have occurred. To arrive at any practical 
results, either diagnostic or curative, we must incise the outer wall through¬ 
out approximately the entire extent of the portion exposed. We must be 
prepared, therefore, to control hemorrhage promptly and effectively as 
soon as the sinus is opened. 

An assistant picks up upon the points of ordinary thumb forceps two 
of the small iodoform plugs, one in each hand. These are held at the upper 
and lower ends of the exposed sinus, but pressure is not exerted until the 
sinus wall has been incised (Fig. 284). With a scalpel the surgeon now 
makes a careful incision—about half 
an inch long—in its outer w T all about 
midway between the compresses. 

This incision is later extended in both 
directions by means of sharp blunt- 
pointed scissors. Unless its lumen 
is actually filled by an occluding 
thrombus at the site of the incision, 
or by thrombi above and below, the 
incision is followed by a gush of 
blood. This is allowed to continue 
for a few seconds in order to gauge 
roughly its volume. This free out¬ 
pouring of blood does not signify that 
a clot does not exist either toward 

the torcular or toward the jugular end of the vessel, foi in either position 
a parietal, non-occlusive clot may be present, and again, even with an 
occluding thrombus toward the torcular end of the vessel, the return flow 
from the inferior petrosal sinus through the jugular bulb will cause very 

copious hemorrhage. 

A few seconds after the sinus is opened, the assistant exerts pressure 



Fig. 284.—Position of gauze plugs for control¬ 
ling hemorrhage when sinus is opened. 






484 SURGICAL TREATMENT OF SINUS THROMBOSIS 


upon its upper (torcular) end. If by this procedure the flow of blood is 
absolutely controlled, we know that the lower end of the sigmoid sinus or 
the jugular bulb is completely occupied by an occluding thrombus; if only 
a little blood trickles through, we know that the jugular end of the sinus 
contains a clot which only partially occludes its lumen. If compression of 
the vessel above exerts no influence upon the hemorrhage, we know that 
the jugular bulb is not occluded, but we do not know nor is it possible 
to determine—that an infective parietal lesion does not exist in that situa¬ 
tion. The assistant now exerts pressure upon the lower, or jugular, end of 
the sinus. This, as a rule, effectually controls the bleeding; or, if bleeding 
continues after compresses have been effectively applied above and below, 
we know that the blood must come from the mastoid emissary entering 
the sinus between them. Let us suppose, however, that all bleeding has 
ceased. The assistant now removes the compress from the upper end of 
the sinus, this, if no clot is present in the lateral sinus, i.e., between our- 
incision and the torcular,—being followed by a renewal of the hemorrhage. 
Should the removal of pressure from the upper end of the exposed sinus be 
followed by no bleeding, this fact would announce to us that the hemorrhage 
had from the first come solely from the direction of the bulb, and from this 
we would deduce the existence of an occluding thrombus in the lateral 
sinus somewhere between the sigmoid bend, or knee, and the torcular. 

It is possible, then, from the simple surgical measures above described 
which, however, require some care and surgical skill in their execution 
to determine the presence of an occluding thrombus (a) at the site of the 
incision, (b) at the jugular end of the sigmoid or within the jugular bulb, 
or (c) at some point within the lateral sinus between the upper exposure 
of the sigmoid and the torcular. Or, by an obviously diminished flow of 
blood from either end, it is possible (but exceedingly rare) that we may be 
able to locate a parietal and only partially occluding clot in one or the other 
situation. We must now outline very briefly the further surgical treatment 
indicated by these various conditions. 

I. Supposing, for example, that cessation of hemorrhage following 
compression at the lower, or jugular, end of the sigmoid, demonstrates 
the presence of an occluding clot somewhere within the lateral sinus: we 
can not from this determine whether the clot is just behind the knee or 
situated at or near the torcular. If we attempt to determine this point, 
and at the same time dislodge the clot, by inserting a curette into the sinus 
and backward in the direction of the torcular, we may fail of our purpose 
and yet inflict injury upon the inner wall of the vessel, leading later to a 
suppurative lesion within the brain itself. It is a more surgical, and there¬ 
fore a safer, procedure to uncover carefully the sinus from the bend back¬ 
ward toward the torcular, splitting the outer wall of the vessel with a 
scissors as we go. Naturally there will be no bleeding until the thrombus is 
reached. It can then be removed cleanly and without injury to deeper 
parts, and the vessel plugged. We then proceed to cut away with scissors 
the outer wall of the sinus on either side of the incision throughout its 


RESECTION OF JUGULAR VEIN 


485 


entire extent. This removes the possibility of pus or other infective matter 
collecting within the lumen of the open and now useless sinus, and creates 
the most favorable condition for a healthy granulating wound. 

Since the presence of a septic clot near the torcular is no proof that 
the jugular bulb is not the site of a second infective thrombus, and since 
also the very opening of the vessel may have paved the way for infection 
below, I am personally in favor of further safeguarding the patient by 
ligating or resecting the jugular vein. 

II. Should absence of hemorrhage from the jugular end of the sinus 
indicate the presence of a thrombus completely filling the jugular bulb, or 
should a greatly diminished blood flow point to a partly obstructive parietal 
clot, I am inclined to believe that we should make no attempt to dislodge 
it until the jugular vein has been ligated. The inferior petrosal sinus is 
presumably still patent, and the attempt to introduce a curette into the 
region of the bulb, if successful in dislodging a clot there, is altogether more 
likely to force it into the general blood stream than to effect its removal 
through the opening in the sigmoid sinus. After the jugular is tied, we 
may make a careful attempt to dislodge the clot from the jugular end of 
the sigmoid, since the blood stream from the inferior petrosal and the 
posterior condyloid vein would then be in reversed direction,— i.e., toward 
and through the opening in the sinus wall. 

III. Supposing that our incision of the sigmoid sinus demonstrates 
the presence of a parietal clot limited in its extent to the site of the incision; 
or, again, supposing that free bleeding occurs from either end, and that 
there are absolutely no physical evidences of a clot or infective lesion in any 
part of the sinus, these negative findings constitute no proof that a focus 
of infection is not present within the bulb or even at the upper end of the 
jugular vein. The logical treatment is, therefore, to compress the sinus 
above and below, cut away its outer wall throughout the entire extent or 
greater part of the portion exposed, pack the wound with iodoform gauze, 
and then ligate or resect the jugular vein. 

I have more than once resected the jugular vein in cases in which no 
positive physical signs of a clot within the sinus could be found, with 
prompt relief of all symptoms of periodic septic absorption. 

Resection of the Jugular Vein. —The rationale of this operation is 
based upon the theory—so far correct—that the elements of infection 
may involve not only the sigmoid sinus and jugular bulb, but also the 
walls of the jugular vein far below its point of exit from the jugular fora¬ 
men. Hence, it is assumed that safety demands in every case its complete 
removal. The correctness of this latter hypothesis is by no means so 
clearly established. 

Preparation .—The side of the neck, from the region of the mastoid 
tip above to the clavicle below, is shaved and thoroughly cleansed. In 
scrubbing this area, all deep pressure or unnecessary manipulation along 
the course of the vein should be avoided, as by this means we might easily 
dislodge a septic clot, which would of course be thrown into the general 


486 SURGICAL TREATMENT OF SINUS THROMBOSIS 


blood current. The cleansing should, therefore, be accomplished with the 
least possible disturbance of the deeper structures. Possibly shaving and 
subsequent painting of the operative field with tincture of iodine may 
prove the ideal preparatory treatment for this particular operation. 

The patient is placed upon his back, with the head turned so that the 
face looks directly away from the shoulder corresponding to the diseased 
ear. A sand-bag wrapped in sterile towels or, if we must improvise, a sheet 
many times folded and rolled into a stout pad, is placed beneath the 
shoulders and neck. This places the sternomastoid somewhat on the 
stretch and also brings the deep structures concerned in the operation into 
more accessible and convenient position. 

Operation (Figs. 285, 286).—The surgical guide for the incision is the 
anterior border of the sternomastoid muscle. The incision begins, there¬ 
fore, at a point corresponding to the 
mastoid tip, or just in front of it, and 
follows the anterior border of the 
muscle downward and forward to its 
clavicular attachment. This incision 
divides the skin and platysma myoides 
muscle, and exposes the anterior border 
of the sternomastoid. In some cases 
the external jugular is large and its 
position such as to require division 
between two ligatures, in other cases 
it is possible to avoid it, and in others 
it is so small that the bleeding is 
easily controlled by artery clamps and 
may not require ligatures. The sterno¬ 
mastoid having been thus exposed to 
view, it is not a difficult matter to in¬ 
troduce a blunt instrument beneath its 
anterior border and deflect it from the fascia upon which it lies. This 
may be easily accomplished with the handle of the scalpel or even with 
the finger. When the muscle has been deflected throughout the extent 
of the incision and drawn backward, the deep fascia is brought into view. 
From this point, it is necessary to work with care and mostly with blunt 
instruments. Having divided the deep fascial layer exposed beneath 
the sternomastoid muscle, we come quickly upon the “common sheath” 
enclosing the jugular vein, carotid artery, and pneumogastric nerve. 
Even before this sheath is opened, the vein is usually easily identified 
by its large size, its prominent position,— i.e., external to the artery,— 
and by its ballooning out with blood when pressure is applied below. 
Before attempting to open the sheath, it should be exposed well 
throughout the length of the incision by deepening the wound in its 
upper portion, where the vessels lie more deeply. The sheath is then 
opened at the lowest point exposed in the wound. This is most 



RESECTION OF JUGULAR VEIN 


487 


easily accomplished by grasping it at two closely approximated points by 
means of two ordinary thumb forceps—great care being taken that only 
the sheath is caught—and tearing it laterally. Once opened, it is not 


Fig. 286.—Internal jugular vein (showing relative position of vein, artery, and nerve). 



difficult to introduce a blunt instrument—preferably a closed blunt- 
pointed scissors curved on the flat—and extend the opening as far upward 
in the neck as the sheath is exposed. 

The next step is the separation of the vein from the artery and nerve. 
This may be effected by means of any blunt instrument. In the lower 
part of the incision, the jugular vein is external to and behind the common 
carotid artery, the vagus lying more deeply between them. It is obviously 
of paramount importance that these structures should be definitely recog¬ 
nized in order that the ligature which is to surround the vein shall not in¬ 
clude the vagus. Having separated the vein from its companion structures, 
two catgut ligatures are passed around its lower part and tied, and the 
vein divided between them. The ligature is cut close upon the lower seg¬ 
ment of the vein, which is allowed to fall back into the wound. The liga¬ 
ture holding the upper segment is, however, often retained for use as a 
retractor. This is given to an assistant, who, by gentle traction in slightly 
different directions, may aid considerably in separating the vein from 
surrounding structures. As the vein is isolated from below upw ard, any 













488 SURGICAL TREATMENT OF SINUS THROMBOSIS 


branches met with are tied between two ligatures and divided. ^ ery 
frequently the lower branches— i.e ., the middle and superior thyroids 
are so small as to be overlooked and torn, in which case the hemorrhage is 
usually insignificant and easily controlled. The common branch of the 
lingual and facial veins is, however, a vessel of considerable size, which 
must be divided between two ligatures. The occurrence of the facial and 
lingual veins as separate branches springing directly from the jugular is 
exceptional. 

It is important that the upper ligature upon the internal jugular should 
be at a point above the facial branch; above the facial branch I do not 
believe, however, that any material advantage is gained by trying to fol¬ 
low the vein as nearly as possible to its point of exit from the skull. 

If the jugular is tied below the point of entrance of the facial, the result 
in many cases will be the control of the disease. There is always present, 
however, the possibility that septic matter—possibly parts of a disinte¬ 
grating thrombus within the bulb—may be washed downward by the blood 
stream from the inferior petrosal, which, finding its way blocked by the 
ligature lower down, may be diverted through the common faciolingual 
branch into other channels, the bacteriaemia being thus perpetuated. 

When all the branches encountered have been ligated, the jugular 
itself may be tied at a point above the facial, and the resected portion 
removed. After its removal, the wound in the neck may be flushed with 
normal salt solution, and its edges approximated and partly sutured, the 
wound being left open above and below, however, for the insertion of 
gauze wicks. 

The mastoid wound is now again uncovered. The gauze plug is re¬ 
moved from the lower end of the sinus, and, if a clot is suspected of being 
present at the point of its entrance into the bulb, a careful and tentative 
attempt may be made to dislodge and remove it. If free bleeding is con¬ 
tinued from the inferior petrosal, a gauze plug must again be applied. If 
absence of hemorrhage points to the presence of clot within the bulb, an 
attempt may be made to dislodge it from its deep position. It must be 
remembered however, that, even if we should succeed in dislodging it, 
the reformation of a clot is under the circumstances inevitable. A wick 
of folded gauze is introduced into the bulb, and the rest of the wound 
packed as after a mastoid operation. 

Usually the gauze compresses used to control hemorrhage may be 
removed on the fourth or fifth day after the operation. If no bleeding 
follows their removal, it is not likely to recur later. 

Obviously complete removal of the jugular is the only operation open 
to us when this vessel is occupied through a considerable portion of its 
length by an organized and presumably infected clot. 

Ligation of the Jugular Vein. — But little need be said as to the 
technic of this comparatively simple operation. As the purpose is to ligate 
the vein above the facial, it is obviously unnecessary to make the long 
incision employed when the vein is to be exsected. An incision beginning 


LIGATION OF JUGULAR VEIN 


489 


at, or in front of, the mastoid tip and extending downward along the an¬ 
terior border of the sternomastoid muscle for a distance of two inches 
should be amply long. If for any reason, as in a girl or young woman, it 
is desired to make the incision as short as possible, it will be found better 
not to attempt to deflect the sternomastoid, but rather to cut directly 
through the muscle, beginning at a point corresponding to the centre of 
the mastoid tip. 

When the jugular has been exposed and isolated at the point at which 
the facial vein is given off, one or both vessels may be tied. If the purpose 
is merely to cut off possible infection from a sinus lesion considerably above 
the jugular bulb, there being no question of disease directly involving the 
jugular itself, ligation of the jugular above the facial vein, and without 
disturbing the latter, would seem to furnish full protection from further 
infection. When, however, the sigmoid lesion is near to or within the 
jugular bulb, and there is some doubt as to whether the infection may not 
have involved the walls of the jugular vein below the facial, the ligation 
of both vessels would seem to be indicated. These, however, are somewhat 
theoretic considerations. When it is necessary to ligate the jugular, the 
additional tying of the facial vein seems so devoid of untoward results, 
that most surgeons will be better satisfied—probably with good reason— 
to have tied both vessels. 

Dr. George L. Tobey, of Boston, has operated successfully upon a 
number of cases of infective sinus thrombosis in which he exposed the vein 
by a very short incision having no apparent relation to the course of the 
sternomastoid fibres. Tobey’s incision through the skin is made parallel 
with some natural fold or crease of the neck, and follows therefore a direc¬ 
tion which crosses the course of the vein. Speaking before the Otological 
Section of the New York Academy of Medicine, he showed a number of 
photographs of patients operated upon by this method, in whom the result¬ 
ing scar seemed hardly noticeable. Certainly from the stand-point of 
cosmetic effect, his results represented a notable improvement upon those 
obtained by the older method. 

When simple ligation of the jugular is spoken of, I assume that this 
means the division of the vein between two ligatures. Having decided 
upon interruption of the blood flow at a certain point, there is obvious 
reason for providing that, should the ligature break down and a suppurative 
lesion be there established, there shall be no chance of this fresh focus of 
infection influencing the general blood stream. 


CHAPTER XVIII. 

SURGICAL TREATMENT OF INTRACRANIAL LESIONS (CONTINUED) .' 
TEMPOROSPHENOIDAL AND CEREBELLAR ABSCESS; 

OTITIC MENINGITIS. 

Surgical Treatment of Brain Abscess.—Up to twenty years ago most 
cases of brain abscess ended fatally. Bezold, 1 writing in 1906, was able 
to say that all the brain abscesses which he had opened had recovered, 



Fig. 287. Relations of brain to temporal bone: a , b, and c, first, second, and third temporal 

convolutions. 


—a fortunate surgical experience to which few surgeons can lay claim. 
The tendency to record successes and forget or ignore failures is so human 
a trait that it is difficult to arrive at correct percentages of deaths and 
recoveries following operation. There is no question, however, that the 

1 Bezold: Text-book of Otol., English Edition, p. 240. 

490 
















PRELIMINARY DISCUSSION OF SURGICAL METHODS 491 


average results of aural brain surgery have been vastly improved during 
the last decade, and I believe that the mortality from otitic brain abscess 
is destined to a further material reduction. 

That there are differences of opinion as to the proper surgical treatment 
of brain abscess is shown by the diversity of methods in use. This diver¬ 
sity is not altogether a result of conflicting views as to how best to arrive 
at a given mechanical result; to some extent it is the expression of widely 
different views as to the tolerance of the brain to surgical manipulation. 

The writer personally believes that, of cases of brain abscess which 
end fatally in spite of surgical intervention, more deaths are due to a faulty 
conception of what the surgeon is called upon to attempt than to a lack of 
operative skill. Before considering the vexed question of operative technic, 
it may be well, therefore, to refer briefly to certain facts bearing upon the 
scope and limitations, as well as the dangers, of surgical intervention. 

In whatever part of the brain the abscess may be located, i.e., whether 
in the temporosphenoidal lobe or in the cerebellum, the main purpose of 
operative intervention is to evacuate pus and provide for subsequent 
drainage. Even when this has been accomplished, however, there are 
certain dangers inherent in the operation itself. Chief among these are 
(a) direct infection of the meninges, (b) the development of a cerebral 
hernia, and (c) intracerebral injuries leading to fresh foci of infection. 

Cerebral Hernice .—Small hernise occasionally contract and disappear 
under proper treatment. Experience has shown, however, that the de¬ 
velopment of a cerebral hernia of any considerable size in cases of otitic 
brain abscess usually foretells a fatal result. The patient may be up and 
about, and for weeks may appear to be progressing satisfactorily toward 
recovery. The protruding cerebral mass prevents local repair, however, 
and subjects the meninges and subdural spaces to constant risk of infec¬ 
tion. The change for the worse is usually sudden, and is not the direct 
result of the hernia itself, but of the diffuse purulent leptomeningitis to 
which it in most cases sooner or later gives rise.. This fact is worthy of 
most serious consideration, since cerebral hernia is to a very considerable 
extent a preventable condition which may be guarded against by proper 
treatment of the dura at the time of the original operation. 

Dural Incision .—In the first place, it should be recognized that there 
is a class of cases in which no incision of the meninges may be necessary. 
Dean 2 proved by the results in his series of cases that a brain abscess 
drained through a “stalk,” or pre-existing sinus, does not usually require 
further opening or even the introduction of drainage tubes or wicks. This 
fact is embodied in a rule or dogma by Heine, 3 to the effect that neither 
puncture nor exploratory incision is necessary when the pus has already 
perforated the dura and can be seen flowing out through a fistulous open¬ 
ing/ ? The truth of this statement seems a logical deduction from the con- 

2 Dean: Operative Procedure for Brain Abscess of Otitic Origin, Annals of Otology. 

vol. xix, No. 3, pp. 541-556. 

3 Heine: Operation on the Ear, English edition, p. 182. 









492 SURGICAL TREATMENT OE INTRACRANIAL LESIONS 


ditions present; for, with such a fistulous opening, we may assume that the 
abscess has existed long enough for the formation of a limiting membrane, 
and also that the contained pus is not under pressure. Rupture into a ven¬ 
tricle is, therefore, not likely to occur. And, again, the adhesive processes 
about the dural outlet will usually have closed the pathways of infection to 
the subarachnoid spa'ce. The development of leptomeningitis is, therefore, 
equally improbable. If we attempt to enlarge the opening, we create gate¬ 
ways of infection. If we are content to facilitate drainage by free removal 
of bone about the dural fistula, we place the patient in the best possible con¬ 
dition for the gradual shrinkage of the abscess cavity with ultimate healing. 

Kdrner, 4 in an analysis of the gross pathologic changes in a series of 
100 brain abscesses, found in 42 cases a fistulous tract directly connecting 
the abscess cavity with the original suppurative focus within the temporal 
bone. In 15 others the brain substance was broken down between the 
abscess cavity and the dura, so that only the dura separated the fistulous 
tract from the diseased bone. 

When no fistulous tract exists, incision of the dura becomes necessary. 
If pathological changes in the dura at some particular point indicate the 
position of a superficial or subdural abscess, the dura should be incised at 
this point. When no such dural changes are present, I believe that the 
dura covering the lateral, or convex, surface of the temporal lobe rather than 
.its under surface— i.e., the dura over the tegmen antri et tympani—should 
be incised, for the reason that the knife carried horizontally into the brain 
explores a larger portion of the suspected region than when it is passed ver¬ 
tically upward from the region of the removed tegmen. A short vertical 
incision through the dura—little longer than the width of a narrow knife- 
blade—is long enough for exploratory purposes, and incurs no risk of 
cerebral hernia. The practice, once rather general, of lifting semilunar 
flaps of membrane in order to expose the brain cortex beneath is happily 
falling into disuse. Aural surgeons now recognize the fact that with brain 
lesions of otitic origin this is not necessary, that it paves the way for un¬ 
manageable cerebral hernise, increases enormously the risks of meningeal 
infection, and does not materially aid the surgeon in locating the seat of 
the disease. I have seen some cases of brain abscess drained after the 
elevation of a dural flap. All ended fatally. 

As to the exploration of a cerebral abscess cavity, it is time that we 
awakened to the fact that any unnecessary disturbance or displacement of 
brain tissue is a technical fault likely to be paid for in terms of human life. 
The practice, once more or less common, of introducing a finger into the 
abscess cavity for the purpose of determining the character and extent of its 
limiting walls, is as illogical as it is dangerous to the patient. If the cavity 
is lined by a distinctly limiting membrane, no therapeutic advantage is 
gained through the information obtained by this method of examination; 
and if no limiting membrane be present, the surgeon will not be able to 


4 Korner: Die otitischen Erkrankungen des Hirns, etc., 1896, p. 97. 









TREATMENT OF BRAIN ABSCESS 493 

distinguish the infected from the surrounding area of healthy brain tissue. 
Furthermore, the introduction of the finger may easily under the latter 
conditions determine a spread of the infection to parts not hitherto in¬ 
volved. In the writer’s opinion, digital examination can not, therefore, 
be too strongly advised against. 

Ballance states that, in cases of brain abscess in which the exploratory 
incisions have failed to release pus, the finger carefully introduced will 
frequently detect an encapsulated abscess as a tense, unyielding mass, 
which may then be opened, the finger being retained in position to guide the 
knife. I can conceive that this 
use of digital examination might 
in some cases serve a useful pur¬ 
pose, though it would seem to me 
a safer method to continue the 
search by multiple incisions or 
punctures. 

The point I wished to make, 
however, is that after a brain 
abscess has been demonstrated 
and partially evacuated by a flow 
of pus along the knife-blade, the 
introduction of the finger into the 
abscess cavity is a useless proced¬ 
ure which may inflict irreparable 
injury upon the brain tissues. 

Operation .—In preparing the 
patient for an exploratory opera¬ 
tion upon the brain, one-half of 
the head should be shaved (Fig. 

288), and the shaved area should 
be cleansed and sterilized by the 
methods already described. 

Frequently the mastoid will 
have been opened previously, so 
that we have only to scrape out and cleanse the old wound and proceed to 
the surgical treatment of the brain lesion. If no previous operation has 
been performed, the mastoid should be operated upon,—a radical operation 
being performed if the suspected abscess be secondary to a chronic middle- 
ear suppuration, the simpler operation of mastoidectomy if the aural lesion 
be acute. 

In operating upon the mastoid of a patient suspected of harboring a 
brain abscess, the use of the mallet and chisel should as far as possible be 
eliminated. This we may usually do altogether in acute mastoid disease 
by biting off the mastoid tip with a rongeur and continuing the removal of 
cortex from below upward with the same instrument. In operating upon 
patients who have suffered from long-standing chronic suppuration, how¬ 
ever, the thickness and density of the bone usually require more or less 



Fig. 288.—Incision for exposing squama, prelimi¬ 
nary to an exploratory operation for brain abscess. 
Upper semicircular incision usually provides adequate 
exposure of squama. The three dotted lines, usually 
uncalled for, give wider exposure if required. 











494 SURGICAL TREATMENT OF INTRACRANIAL LESIONS 


use of the chisel or gouge. The objection to these instruments depends, 
of course, upon the possible effect of the resulting concussion upon a col¬ 
lection of pus, perhaps under pressure, within the brain. 

The operation upon the mastoid should be performed as quickly as 
possible. All diseased masses of bone should be dealt with radically. 
The bony plate forming the roof of the mastoid cavity should be scraped 
clean of diploic tissue. These essentials having been accomplished, we 
should waste no time on minor operative details, which may be left to 
subsequent operation should the need arise. Having exposed the inner 
plate forming the floor of the mid-cranial cavity, this should be carefully 
scrutinized for necrotic defects through which pus may be seen escaping 
from the cranial cavity. Failing to find a fistula leading into the brain 
cavity, the roof of the mastoid should be removed, and the dural surface 
thus exposed examined for either a fistulous opening or for pathologic 
changes indicating a subdural abscess or the subdural terminal point of a 
fistulous tract leading into the brain substance,— i.e., to a brain abscess. 

Treatment of a Brain Abscess Drained through a Dural Fistula .—Should 
a fistulous opening be found in the dura over the roof of the mastoid, or for 
that matter in any situation, and pus be seen escaping therefrom, we should 
consider ourselves fortunate in having discovered a condition which offers 
a comparatively favorable prognosis. No attempt should be made to 
enlarge the dural opening. The dura surrounding the fistula should be 
exposed by the free removal of bone. Fistulous tracts generally do not 
tend to rapid closure so long as they form the principal pathway for escap¬ 
ing pus. We should not, therefore, attempt to improve upon Nature’s 
provision for drainage,—at least, until it shall have been proved inade¬ 
quate. The depths of the mastoid wound, and especially the region of 
the aditus, should be firmly packed with iodoform gauze, while folds of 
plain sterile gauze should be placed against the dural surface and fistula, 
and the usual outer mastoid dressing applied. 

The dressings should be changed daily. Naturally, any change or 
recurrence of constitutional or focal symptoms— e.g., temperature or pulse 
changes, head pain, insomnia, mental obscuration, aphasic symptoms, in 
short any phenomena which might point to intracranial pus retention— 
should be looked for and noted. 

At the daily changes of dressing, any changes in the condition of the 
dural fistula should be noted. Our problem here is to maintain the 
patency of the dural opening. If, therefore, there are physical evidences of 
its premature closure, we may combat this by the introduction of a small 
folded gauze wick. What is hoped for, and what probably actually occurs 
in favorable cases, is the gradual obliteration or shrinkage by cicatricial 
contraction of the abscess cavity or tract from its depth outward to the 
dural opening. After this process is completed, there can be no further 
escape of pus, and spontaneous closure of the dural opening follows. 

Naturally, if the surgeon’s zeal leads him to persist in introducing drain¬ 
age tubes or wicks deeply into the fistulous tract, spontaneous healing 
cannot occur. In a series of ten cases operated upon for brain abscess, 


EXPLORATION OF BRAIN 


495 


Dean found three with pus escaping through fistulous openings in the 
dura. In one the dural opening was not enlarged, but a gauze wick was 
introduced. In the other two the fistulous tracts were absolutely depended 
upon to maintain drainage, not even the smallest wick being introduced. 
All of the three cases made perfect recoveries. 5 

Exploration of the Brain .—The mastoid roof having been removed, and 
no fistulous tract or necrotic area of dura being present, the temporal 
lobe should be further exposed by removal of a portion of the squama. 
This may usually be rapidly accomplished by means of a stout rongeur, 
beginning just above the mastoid and biting away the squama until an 
area of dura about equal to that shown in Fig. 289 is uncovered. While 



Fig. 289.—Dural exposure preliminary to exploration of the brain for suspected temporosphenoidal 

abscess. 

this may be done by mallet and chisel, it is particularly important to avoid 
the jar caused by these instruments in the neighborhood of a suspected 
brain abscess. An area measuring roughly about V /2 inches laterally by 
1 inch in height provides a sufficient initial exposure. 


5 Dean, L. W.: Brain Abscess of Otitic Origin, Annals of Otol., vol. xix, No. 3. 

































496 SURGICAL TREATMENT OF INTRACRANIAL LESIONS 


Before opening the dura, the whole wound should be flushed with 
normal saline solution. The mastoid wound and particularly the region 
of the aditus should be firmly packed with iodoform gauze. The towels 
about the wound should be changed. A little peroxide of hydrogen may be 
poured over the exposed dura, which may then be covered with gauze 
moistened in 1 to 4000 bichloride solution. The surgeon s hands should 
be re-sterilized, or, if wearing gloves, these should be changed. All in¬ 
struments previously used should be removed and only freshly sterilized 
instruments should be used in the actual exploration of the brain. 

For exploring the brain the aspirating needle is not a reliable instru¬ 
ment, as its lumen may become occluded by brain tissue, and, even when 
this does not occur, it may fail to give passage to thick pus. A more effec¬ 
tive instrument is the narrow blade of a long straight bistoury (Fig. 290). 



Fig. 290.—Narrow-bladed knife for exploring the brain (size and length reduced). 


For one’s initial puncture, the logical point of attack is just above the 
tegmen tympani (Fig. 289, a ). Holding the knife with the blade surface in 
the vertical plane,— i.e., with cutting edge directed either upward or down¬ 
ward,—it is introduced directly into the brain substance in a direction at 
right angles to the anteroposterior plane of the skull. Introduced in this 
way, the knife makes a short vertical incision through the dura which, 
whether an abscess is or is nob encountered, is not likely to give rise to a 
cerebral hernia. The knife should enter the brain slowly, its progress being 
arrested frequently— i.e., at distances of 5 or 6 mm.—and the blade slightly 
rotated to favor a possible escape of pus. The advantage of this gradual and 
interrupted introduction must be apparent; for, if we quickly plunge the 
knife to what we believe to be the limit of safety and an escape of pus fol¬ 
lows, we shall be left in doubt as to the depths at which the abscess was 
reached. If the knife is arrested at a depth of 5 to 6 mm. and pus escapes, 
we shall be in no doubt as to the superficial character of the lesion, whereas 
an escape of pus occurring only after it had been introduced to the limit of 
safety would constitute fairly positive evidence of a deep-seated abscess. 

If the knife, introduced, as above described, to a depth of one and a 
half inches, fails to draw pus, it should be withdrawn and reintroduced in 
the same careful way at a point about three-eighths of an inch behind the 
first (6). This also failing, the next incision may be made at a point three- 
eighths of an inch in front of the initial puncture (c). It must be remem¬ 
bered that classical focal symptoms of brain abscess have frequently been 
proved post mortem or by operation to have depended upon very small 
pus collections; and, further, that, while the most frequent seat of otitic 
brain abscess is the region in close proximity to the tegmen tympani, such 



EXPLORATION OF TEMPOROSPHENOIDAL LOBE 497 


an abscess may occupy any position within the temporosphenoidal lobe. 
It may be necessary, therefore, to make a number of closely approximated 
parallel incisions in order to locate a small abscess giving definite symptoms. 

The practice which I have seen advocated, of introducing the knife 
a second or even a third time through a single dural incision in order to 
explore the brain in different directions, is clearly inadvisable, for the fol¬ 
lowing reasons : (1) The dural incision itself, provided that perfect 

asepsis has been maintained, involves little danger; (2) should infection 




Figs. 291 and 292 are drawings made from a section of the brain, and show schematically the 
advantages of exploring the brain through separate incisions of the dura as compared with exploratory 
punctures in different directions through a single dural incision. In figure 292 the arrows indicate 
possible avenues of pus from an evacuated abscess to new foci of infection. 

occur later, and pus escape from a dural incision through which the brain 
had been punctured in different directions, we would be at sea as to the 
site of the focus of infection; and (3) should the second or third introduc¬ 
tion of the knife through a single dural incision reach the abscess sought for, 
the pus thus evacuated would pass at the dural outlet the open mouths of 
the tracts made by the first exploratory incisions, and might easily lead 
to fresh pathways and foci of cerebral infection. This point is made clear 
by Figs. 291 and 292, in which the possible results of separate incisions 
and of multiple punctures through a single dural incision are compared. 

32 



















498 SURGICAL TREATMENT OF INTRACRANIAL LESIONS 


Surgical experience has abundantly proved that incision of the dura 
under aseptic precautions does not per se involve any very serious danger. 
Some years ago the writer performed an exploratory operation upon a 
woman suspected of harboring a brain abscess. Though no abscess was 
found, the woman made a rapid recovery, without at any time showing 
symptoms referable to the three incisions through the meninges. A cere¬ 
bellar abscess operated upon by the writer was evacuated only by the 
fourth incision, the patient recovering without having exhibited any symp¬ 
toms traceable, to the four dural incisions. A case still more graphically 
illustrating the tolerance of the meninges to aseptic surgery is that of a 
brain abscess reported some years ago by Dr. John R. Page. 6 In this case 
the symptoms pointed strongly to a cerebral abscess, which was finally 
located and evacuated only after sixteen separate incisions into the brain 
substance had been made, the patient making a perfect recovery. These 
cases are cited for the purpose of emphasizing this point, — viz., that, 
having sufficient grounds for an exploratory operation upon the brain, 
one should not hesitate to make as many incisions through the meninges 
and into the brain substance as may be necessary either to locate the ab¬ 
scess or to furnish fairly conclusive evidence of its absence. 

The three incisions (a, 6, and c, Fig. 289) having failed to locate the 
abscess, a second row of incisions above those first described should be 
made. These also failing, the brain in front of and behind the area indi¬ 
cated above should be explored. This may require an even more extensive 
removal cf bone. This, though to be regretted, can not be weighed against 
the possibility of leaving without external outlet a collection of pus within 
the brain. 

Depth of Exploratory Incisions into the Brain. — Naturally, when a 
brain abscess is present, the puncture of a ventricle might determine a 
rapidly fatal result by creating a passage along w r hich the abscess might 
expel its contents into the ventricle. While I have seen no record of such 
an accident as a result of an exploratory operation, it is well that such a 
possibility should be borne in mind. The anterior and posterior horns of 
the lateral ventricle are in relation respectively to the frontal and occip¬ 
ital lobes rather than to the temporal or parietal. They are on a level 
from \y± to 2 inches above that of the tegmen tympani, and are at least 
2 x /i inches respectively from the upper anterior and upper posterior cor¬ 
ners of the dural exposure shown in Fig. 289. In a case of serous menin¬ 
gitis in which from a very similar exposure I intentionally punctured the 
posterior horn, it seemed to me that the instrument was inserted to a 
depth of at least 2% inches before the volume of escaping liquor cerebri 
showed that the ventricle had been reached. Why a direct puncture— 
i.e ., horizontally inward—of the temporal lobes from a point about % to 1 
inch above the tegmen tympani should not reach the inferior horn of the 


6 Page: Report of a Case of Brain Abscess, etc., Amer. Journal of Surgery, Septem¬ 
ber, 1908. 



DRAINAGE OF BRAIN ABSCESS 


499 


lateral ventricle, I do not know. Personally I should feel it necessary to 
proceed very cautiously at this point after the knife had been carried to a 
depth of l}/i inches. Heine, in discussing the safety limit as to the depth 
of exploratory punctures, quotes Korner as placing 4 cm. (about 1% inches) 
as the limit of safety. Heine, however, cites a case operated upon by him¬ 
self in which an abscess was reached only at a depth of 7 cm. (about 2% 
inches) from the exposed dural surface, and states his belief that, in the 
nature of the lesion, it is essential that one be not too closely bound by 
dogmatic rules as to the position of important structures and their rela¬ 
tion expressed in millimetres to the cerebral cortex. 

Drainage .—A brain abscess having been opened, whatever subsequent 
treatment will maintain the patency of the drainage pathway and at the 
same time subject both brain and meninges to minimum disturbance and 
manipulation, will in the long run secure the best average results. 

Irrigation of the abscess cavity, while it has been successfully used in 
certain cases, is a measure not of itself without possibilities of harm, and 
is no longer advocated. 

The practice of making a crucial incision of the dura is not essential to 
adequate drainage. By weakening the dural support, it may pave the 
way for a small hernia cerebri, and to this extent certainly increases the 
risk of subsequent meningeal infection. 

On no account should the finger be introduced into the freshly made 
tract by which the abscess is being drained. 

If the surgeon is convinced of the necessity of mechanically aiding in 
the removal of pus, Whiting’s encephaloscope (Fig. 293) may be carefully 
introduced, and pus as it flows into the lumen of this speculum may be 
wiped out by means of cotton-tipped applicators. But to feel that one is 
called upon to explore the nooks and corners of the abscess cavity by means 
of this or any other instrument is likely to lead to the infliction of mechan¬ 
ical injuries, possibly giving rise to fresh pathways or foci of infection. 

Having created an avenue of escape,—presumably a path of least 
resistance,—the most important agency in maintaining adequate drainage 
is the evenly distributed force of normal intracranial pressure. Suppose, 
for example, in a given case that diverticula containing pus do exist. 
Presumably they were caused by pus under pressure seeking escape. 
Pressure within the abscess cavity having been relieved by a newly made 
pathway of escape, it seems not illogical to expect upon purely physical 
grounds that small communicating spaces containing pus may drain back 
into the main abscess cavity and not refill so long as the outlet of escape is 
maintained. I believe, therefore, that we should not attempt to explore 
by actual touch or sight the brain abscess which we have just succeeded 
in opening. 

When pus following the knife shows that the abscess has been located, 
it should be held steadily in place and slightly rotated until pus ceases to 
flow. It may then be used as a guide for the introduction of whatever 
instrument is to take its place or for the permanent wick or drain. 


500 


SURGICAL TREATMENT OF INTRACRANIAL LESIONS 


If the abscess is deep-seated, Heine advises that drainage be main¬ 
tained by a piece of perforated rubber tubing, wrapped in iodoform gauze 
and introduced not too deeply into the abscess cavity. Theoretically such 
a drain would seem to the writer to involve considerable risks in the 



Fig. 293.—Whiting’s encephaloscope. 


mechanical irritation to which it might give rise. The use of absorbable 
decalcified chicken bone, which was emploj^ed so successfully by Macewen, 
is open to certain obvious objections, and is not in general favor to-day. 
McKernon’s choice— i.e., of a cigarette gauze wick rolled in a mixture of 













DRAINAGE OF BRAIN ABSCESS 


501 


equal parts of powdered boric acid and iodoform—gave excellent results 
in a series of cases operated upon by him. 

As to the problem of keeping the drain or wick in proper position, the 
writer learned a simple expedient from the following probably fairly com¬ 
mon experience. In making the first change of dressings in an abscess case, 
the gauze wick was found lying flat upon the dural surface, having been 
expelled by intracranial pressure. To ensure against a repetition of this 
mishap, he had a number of wicks prepared in the following way: First, 
a small flat pad of three or four folds of gauze was made. With the pointed 
blade of a scissors a small hole was made in the centre of this pad, and 
through this a loop of infolded gauze 
wick was forced (Fig. 294). A number 
of these were prepared and sterilized, 
each in a separate wrapper. In actual 
use they seemed to have the following 
advantages: (1) Having determined 
the depth to which we wish the wick to 
penetrate the brain,—-say one inch or 
an inch and a quarter,—the loop of 
gauze wick is forced through its fix¬ 
ating pad to this length. When this 
loop-wick has been introduced into the 
abscess cavity, the pad is flattened 
against the surrounding dural surface 
and sterile gauze is packed around it. 

In this way the wick is held immovably 
in place and by a means which in no 
way interferes with drainage and can¬ 
not possibly produce irritation of sur¬ 
rounding tissues. (2) Having thus to 
arrange in advance the length of each 
wick introduced, the surgeon is never in 
doubt as to the depth to which the 
wound is being packed, and he is in a position to arrange systematically for 

a gradual and progressive shortening of the wick. 

^ Many surgeons prefer to provide drainage in brain abscess cases by 
means of a small flattened roll of sterilized rubber tissue, claiming an ad¬ 
vantage in the smoother surface as less likely to irritate contiguous 

brain tissue. . 

Personally, I believe that the dressings in brain abscess cases should 

be changed daily, the saturated wicks being removed and dry sterile ones 
replaced with the least possible friction or mechanical disturbance of the 

tissues involved. . Al . „ 

Should an occasional escape of pus seem in excess of that usually com¬ 
ing away with the change of dressings, this of itself should not be regarded 
as an indication for further exploration or subdural manipulation of the 



Fig. 294.—Gauze wick for use in brain 
abscess. Only the loop (a) is introduced 
into the abscess tract and cannot, therefore, 
leave threads behind it on withdrawal. The 
length can be regulated at will, and when 
gauze is packed around the fixation pad, the 
wick cannot be displaced or expelled by in¬ 
tracranial pressure. 











502 SURGICAL TREATMENT OF INTRACRANIAL LESIONS 

brain. Having established drainage, and the symptoms of intracranial 
disturbance having subsided, I believe that nothing short of a recurrence of 
svmptoms pointing to pus retention should tempt the surgeon to a further 

exploration of the interior of the brain. 

Finally, it is of the greatest importance that the patient—however 
favorably he may appear to be progressing toward recovery—should for a 
considerable period be kept absolutely quiet in bed. The surgeon should 
be in no hurry to close the wound. The two chief dangers of the post¬ 
operative period—viz., secondary retention of pus within the brain and 
late infection of the meninges—are always present during the first weeks 
following the operation. Until the period of postoperative danger is 
definitely passed, the patient should be kept quiet in bed and guarded 
against any indiscretion which might turn the scale unfavorably against 
recovery. 

Cerebellar Abscess. — The surgical treatment of cerebellar abscess 
is practically the same as that of abscess of the temporal lobe. Since an 
epidural abscess if present is most likely to be found in close relation to 
the posterior surface o ( the petrous bone, the cerebellar dura should first 
be exposed in this situation. 

This is best done by uncovering first the sigmoid sinus, and then with 
a suitable rongeur removing the bone in front of and internal to its anterior 
border. When sufficient bone has been removed, we have an exposure of 
cerebellar dura throughout a triangular space bounded above by the tegmen 
antri, behind by the anterior margin at the sigmoid sinus, and in front by 
the petrous bone (Fig. 297, a). 

Should a fistulous opening in the dura be present in this area, it should 
be treated by exactly the same conservative method as that already 
advised in the case of temporal lobe abscesses drained through pre-existing 
dural fistulse. 

As in the case of temporal lobe abscess, the dura, though intact, may 
show pathologic changes indicating the site of a subdural collection of pus 
or the subdural terminal point of a necrotic tract leading to a cerebellar 
abscess. 

Even though no such pathologic changes are present, an effort may be 
made to locate the abscess through the dural exposure in front of the sinus. 
Before incising the dura, the wound should be cleansed, the aditus firmly 
packed with iodoform gauze, fresk towels placed about the wound, and 
the surgeon’s hands re-sterilized. 

In the first incision the knife is carried directly inward to a depth of 
not more than one inch (Fig. 295, a). This failing, a second incision, 
made through a separate dural opening behind the first, is carried inward 
and slightly backward to a depth of 1%,—not more than \ x /± inches (6). 
Should this also not give exit to pus, it is better that no further effort be 
made to locate the abscess from this exposure. The mastoid wound is 
now packed with iodoform gauze, plain sterile gauze, however, being- 
placed against the incised dura. 


TREATMENT OF CEREBELLAR ABSCESS 


503 


It is now necessary to expose the cerebellum behind the sigmoid sinus 
by a removal of bone from that part of the occipital bone forming the 
outer wall of the cerebellar fossa. This may be done by trephining at a point 
one inch behind the centre of the sigmoid sinus and well below the level 
of the lateral sinus; or, better, by means of a stout rongeur we may con¬ 
tinue the removal of bone directly backward from the posterior border of 
the sigmoid sinus. The results of 
the two methods of exposing the 
occipital aspect of the cerebellum 
are shown in Figs. 296 and 297. 

In these illustrations the sigmoid 
sinus is shown somewhat dia- 
grammatically. That is to say, 
the bony support having been 
removed, the rounded contour of 
the sinus is usually lost, and the 
line of demarcation between the 
dura covering the sinus and that 
covering the cerebellum is, there¬ 
fore, not so clearly defined as 
appears in the illustrations. 

The posterolateral aspect of 
the cerebellum having been ex¬ 
posed, we should adopt some sys¬ 
tematic plan of completing the 
search for the suspected abscess. 

As with the temporal lobe, each 
exploratory puncture should be 
made through a separate dural 
incision. The first, incising the dura well forward, enters the cerebellum 
in a direction inward and strongly forward, and to a depth of one inch 
(Fig. 295, c). The next incision, cutting the dura a little behind the first 
opening, passes inward and slightly forward to a depth of 1H inches ( d ). 
This also failing to draw pus, a fifth incision ( e) is carried directly 
inward through the posterior part of the cerebellum to a depth of 
1 y 8 to 1M inches. 

The writer some years ago performed an exploratory operation upon 
the cerebellum which failed to locate an abscess. The autopsy, made by 
I)r Zabriskie, showed a small, deep-seated abscess to ha\e been present, 
and that one incision, which traversed the cerebellum in the right direc¬ 
tion, had failed by an eighth of an inch to enter the abscess cavity. Realiz¬ 
ing that this failure was in some degree due to a lack of adequate knowl¬ 
edge of cerebellar measurements, the writer has had forcibly impressed 
upon him the importance of systematic method and thoioughness in an 
operation of this nature. Fig. 295 represents an effort to place at the 
student’s disposal a chart giving approximately the directions and depths 








504 SURGICAL TREATMENT OF INTRACRANIAL LESIONS 


of exploratory punctures of the cerebellum which should fairly well cover 
the region to be explored. If these several efforts fail to locate the abscess, 
and the surgeon is still uncertain as to its possible presence above or below 
the plane of the incision herein described, one or more supplementary in¬ 
cisions above and below may be made. 



Pig. 296.—Exposure of dura covering cerebellum: d, supplementary skin incision for adequate 
exposure of bone; a, cerebellar region in front of sigmoid sinus; b, sigmoid sinus; c, cerebellar 
region behind the sigmoid sinus. 


The abscess having been located, the subsequent drainage and the 
after-treatment may be carried out by practically the same method as has 
been described in connection with abscess of the temporal lobe. 

Meningitis.—The surgical treatment of otitic meningitis has already 
been discussed in connection with the pathologic and clinical aspects of 
the various recognized types of the disease. All that is called for here, 
therefore, is a very brief resume of the different surgical procedures which 
have proved their value in certain cases, and of the not too clearly defined 
indications for their use. 

Serous Meningitis: Treatment .—All that may be necessary is a very 
careful and rather wide uncovering of the dural area involved. Particularly 
in children are symptoms of marked meningeal irritation frequently relieved 
by this comparatively simple operation. Unless the symptoms or the patho¬ 
logic changes in the bone suggest the posterior fossa as the probable seat of 
the meningeal lesion, the dura covering the temporal lobe should be first 
exposed. This may be done in exactly the same way as the preliminary 
exposure for exploring the brain in a case of suspected temporal lobe 















TREATMENT OF SEROUS MENINGITIS 


505 


abscess,— i.e., the tegmen tympani et antri is first removed and then the 
adjacent portion of the superior plate of the squama. The writer recalls 
the case of a child who, following a simple mastoid operation, developed 
high fever, continuous at 104° F. or thereabout, rigidity of the neck muscles, 
delirium, and strabismus, all of which disappeared within a few days after 
the operation referred to above. 

Should the surgeon have reason to fear that the cerebellar dura is the 
seat of trouble, this region also should be exposed by a removal of bone 
just in front of the sigmoid sinus (see Fig. 297). 



Fig. 297.—Exposure of dura covering cerebellum : a, cerebellar region in front of sigmoid sinus; 

b, sigmoid sinus ; c, cerebellar region behind sigmoid sinus. 


Simple uncovering of the dura is particularly indicated in the case of 
young children, who are more prone than adults to the development of 
mild forms of meningeal inflammation, and whose symptoms are also 
likely to be far more pronounced. I believe also that it should be used as 
a preliminary measure in all comparatively mild cases, whether occurring 
in children or adults, in which lumbar puncture fails to reveal pus or bac¬ 
teria in the spinal fluid. If successful, there is usually some amelioration 
of symptoms or improvement in the patient’s general condition within 
twenty-four hours. If no improvement is realized, the operation may then 
be quickly and easily supplemented by one or more incisions of the dura. 

The above statement refers to cases of serous meningitis of moderate 
or average severity. Undoubtedly there are cases in which the symptoms 
assume early so alarming a type that one is impelled at once to adopt 
more radical measures. When, following symptoms of meningeal irrita¬ 
tion, the patient quickly lapses into delirium and shows the peculiar 
depression of the vital forces characteristic of grave meningeal disturbance, 
there should be no loss of time in relieving tension by several incisions 
through the dura. 

Puncture of the Lateral Ventricle. — Withdrawal of fluid by lumbar 
puncture has been advised as a means of obtaining prompt relief of pres- 














506 SURGICAL TREATMENT OF INTRACRANIAL LESIONS 


sure in severe cases. The exact indications for this procedure have not 
yet been determined. The writer has had under his care one apparently 
hopeless case of serous meningitis (see pages 390-391) in which tapping 
of the ventricle was followed by almost spectacular relief of symptoms. 
While the result in this case was most gratifying, there has always existed 
a doubt in the writer’s mind as to whether the ultimate result might not 
have been the same had he limited the extent of his intervention to the 
three vertical incisions of the dura which formed part of the operation. 

Serous Meningo-encephalitis (Korner). — This condition, prob¬ 
ably analogous in its origin and inception with serous meningitis, differs 
chiefly in the extension of the morbid changes into the substance of the 
cerebral cortex. In some cases the outer brain structures bear the brunt 
of the attack, the symptoms suggesting a cerebral rather than a meningeal 
lesion. Such cases have been reported by Jansen, Arnold Knapp, the 
writer, and others (see cases cited in Chapter XIII). 

The surgical treatment of otitic serous encephalitis begins by exposure 
of the dura covering the temporosphenoidal lobe as for an exploratory 
operation for brain abscess (Fig. 289). Under the strictest aseptic pre¬ 
cautions, two or three parallel vertical incisions through the dura, and 
passing to a depth of a half inch directly into the brain substance, are made. 
No drains should be introduced for the purpose of maintaining the patency 
of these openings. Rather loose folds of sterile gauze are placed against 
the incised dura. In favorable cases the improvement in the patient’s 
condition is soon noticeable, and the symptoms, once relieved, do not, as a 
rule, recur. Following this operation there is likely to be a rather copious 
leakage of cerebrospinal fluid into the dressings, which may persist, but 
in gradually diminishing amount, for two or three weeks. 

Should the meningeal symptoms, having once definitely subsided, 
recur, their reappearance will usually be found to depend upon the develop¬ 
ment of diffuse suppurative leptomeningitis. The importance of main¬ 
taining the most careful asepsis during the postoperative period must, 
therefore, be apparent. 

Purulent Leptomeningitis. — The surgical treatment of purulent 
leptomeningitis, circumscribed or diffuse, may be dealt with briefly. The 
dura covering the under and lower-lateral surface of the temporosphenoi¬ 
dal lobe should be exposed; and unless there is physical evidence that the 
disease is located there, the cerebellar dura should also be uncovered by 
the removal of bone in front of and internal to the sigmoid sinus. The 
exposed dura in both regions should be closely scrutinized for physical 
evidences of disease. When inflammatory changes confined to a limited 
area point with probability to the existence of a circumscribed leptomenin¬ 
gitis, the area involved should be freely incised in parallel lines. Unless 
the meningeal lesion is complicated by a subdural collection of pus of 
appreciable size, drainage wicks should not be introduced. Sterile gauze 
in loose folds is placed against the dural incisions, and a large absorbent 
dressing applied. The dressing should be changed daily, the frequent 


TREATMENT OF PURULENT LEPTOMENINGITIS 507 


removal of surface pus and pus-soaked gauze being necessary to promote 
drainage. When it is deemed necessary to maintain mechanically the 
patency of the dural openings, the lips of the incisions may be separated 
occasionally by means of a grooved director or other blunt instrument. 
As a rule, this is not necessary. 

When the macroscopic changes in the dura and the symptoms both 
point to the presence of a diffuse or spreading suppurative leptomenin¬ 
gitis, the lesion, so far as our present knowledge goes, is a hopeless one. 
Usually the character of the changes is such as will not be relieved by drain¬ 
age, and furthermore the area involved is too extensive to be reached by 
any operative procedure. While the prognosis is, therefore, most unfavor¬ 
able, I believe in giving the patient the benefit of any theoretic chance. 
The dura of the temporosphenoidal lobe should, therefore, be freely drained 
by multiple incisions. Regarding 'the disease as having some analogy 
with other suppurative lesions, the above treatment is at least in accord 
with surgical principles. The postoperative treatment is the same as for 
circumscribed purulent meningitis,—daily very careful renewal of the 
dressings. 

The puncturing of the lateral ventricle in diffuse purulent leptomen¬ 
ingitis does not appeal to me as a rational or promising measure. 


CHAPTER XIX. 

FACIAL PARALYSIS. 


Facial paralysis of otitic origin may result from any of the following 

conditions: (1) Acute suppurative otitis media of severe type, the inflam¬ 
matory process extending through the tympanic wall of the Fallopian 
canal, and the nerve being either directly involved or subjected to pres¬ 
sure by inflammatory products within the canal. This is commoner in 
young children than in adults. (2) During acute suppurative otitis media 
as a result of direct exposure of the nerve through a defect in the tympanic 
wall of the facial canal. (3) In chronic suppurative otitis media, the 
necrotic process involving the facial canal. (4) In suppurative labyrinth¬ 
itis secondary to chronic middle-ear suppuration, a necrotic tract through 
the horizontal semicircular canal may by downward extension involve the 
facial. (5) Facial paralysis is an occasional accompaniment of otitic 
meningitis, in which case the nerve lesion is probably more often the result 
of an intermediate infection of the labyrinth than of an extension of inflam¬ 
mation from the meninges to the nerve-trunk as it traverses the internal 
auditory canal. (6) Tuberculous lesions. In a very large precentage of 
cases of middle-ear tuberculosis, the facial nerve is involved. A tuber¬ 
cular element in the pathogenesis of facial paralysis is recognized as 
affecting the prognosis unfavorably, from the greater frequency with 
which the nerve is actually destroyed. (7) Herpes zoster auriculae (Hunt) 
is an occasional cause of facial paralysis. In this affection the morbid 
changes in the nerve are clearly an extension of the inflammatory process 
primarily affecting the geniculate ganglion. 

Generally speaking, facial paralysis resulting directly from middle-ear 
or mastoid suppuration—the labyrinth having escaped infection—offers, 
under prompt and rational treatment, a prefectly favorable prognosis. 
Usually all that is required to effect a cure is careful removal of all diseased 
bone through a simple mastoidectomy or radical operation, according to 
the nature of the tympanic lesion. 

Postoperative facial paralysis may occur: (a) as the immediate result 
of division or injury of the nerve during a radical operation: or (b) as the 
deferred result of a slight traumatism, the paralysis appearing only after 
an interval of several hours or days has elapsed, (c) When the tympanic 
wall of the facial canal is either defective or unusually thin, paralysis' . 
may result directly from the pressure of a gauze dressing packed too tightly 
into the wound cavity, (d) A thick-walled, sclerotic mastoid with a very 
small, deeply-placed antrum is a type of bone in which during a simple mas¬ 
toidectomy great care may be necessary to avoid injury to the nerve. The 
danger in this type of bone lies in the fact that the uniform or average density 
of bone is such as to obscure certain common surgical landmarks, and in the 
508 


SYMPTOMS; PHYSICAL SIGNS 


509 


search for a small antrum—often hardly extending beyond the usual confines 
of the aditus—the nerve is injured before the surgeon recognizes the surgical 
region he has reached. A particularly distressing feature of an accident to 
the nerve occurring in this way is the fact that the injury is likely to be com¬ 
plete, and the resulting paralysis therefore permanent. The deduction from 
this statement is practical and clear: i.e., that the surgeon, having recog¬ 
nized the type of bone he has to deal with, should either proceed with un¬ 
usual and infinite care, or make use of the postero-superior wall of the bony 
auditory canal as a guide to the aditus and antrum. It is better to sacrifice 
any non-vital structure than permanently injure the facial nerve. 

The regions in which the nerve is most likely to be injured were spoken 
of in connection with the technic of the radical mastoid operation (page 
442), and need not be referred to here. 

Symptoms and Physical Signs. —The facial changes accompanying 
this lesion are so characteristic and constitute a deformity so pathogno¬ 
monic as to overbalance in diagnostic importance all other clinical features. 

Owing to the paralysis of the facial muscles corresponding to the side 
of the aural lesion, the normal facial folds are obliterated. Thus the 
wrinkles or lines of the forehead and about the eye and the nasolabial 
fold disappear wholly. The skin, therefore, presents a smooth and line¬ 
less surface in conspicuous contrast to the opposite side of the face. In 
children and young adults this may not be conspicuous while the face is 
in repose, but becomes unpleasantly noticeable as soon as the sound facial 
muscles are called into activity,— e.g., in laughing, crying, etc. The patient 
cannot close the eye on the affected side, and cannot contract the labial 
muscles. In cases of complete paralysis, the affected side of the mouth 
may droop to such an extent as to allow a more or less constant escape 
of saliva. 

As a result of the physical changes above noted, the patient may experi¬ 
ence the following disturbances of the special senses: The inability prop¬ 
erly to close the eyelids leaves the eye unprotected, and the conjunctiva 
and even the cornea may become inflamed or congested. Owing to paraly¬ 
sis of the nasal muscles and collapse or flaccidity of the ala nasi, the pas¬ 
sage of air to the upper nasal chamber is diminished or prevented, and to 
this extent the olfactory sense is disturbed. Paralysis ol the chorda 
tvmpani nerve is responsible for loss or disturbance ol taste in the coi 1 e- 
sponding half of the tongue. Finally, paralysis of the stapedius may result 
in a very annoying disturbance of the auditory function, which takes the 
form of a loss of auditory balance or power of accommodation to various 
sounds rather than of an actual diminution of hearing. In many cases 
the paralysis of the stapedius in persons whose hearing has previously 
not shown great impairment is said to result in an appreciable hypei acusis 
for the lower musical tones. 

The recognition of these various disturbances of the special senses is 
said in some cases to be of value in determining the location ol the suigical 
injury to the nerve. Thus, division of the nerve within the facial canal at 



510 


FACIAL PARALYSIS 


a point between its exit at the stylomastoid foramen and the point at which 
the nerve to the stapedius is given off, would involve the chorda tvmpani 
and cause disturbances of taste, but would not give rise to any disturbance 
of the auditory function. Division of the nerve above the branch to the 
stapedius would add to those just mentioned the symptoms of disturbed 
audition,— i.e., some confusion of sound impressions, hyperacusis for the 
lower tones, tinnitus aurium, etc. 

When the paralysis is complete and attended by characteristic elec¬ 
trical reactions of degeneration, marked atrophy of the paralyzed facial 
muscles may add to the disfigurement. 

Prognosis. —The prognosis depends upon the character of the injury. 
Actual division, unless the segments are maintained in apposition or are 
subsequently reunited, means permanent paralysis. When the nerve is 
not actually divided, recovery, partial or complete, occurs in the great 
majority of cases. As to the duration of the paralysis in any particular 
case, but little can be said. A paralysis due to pressure may recover 
completely within a few weeks, whereas a lesion due to a severe traumatism, 
giving rise to complete degeneration of the peripheral segment, may cause 
a paralysis lasting a year or more and yet result ultimately in complete 
recovery. 

Treatment. —When there is no reason to fear that the nerve has been 
actually divided, the patient should be told that ultimate recovery is to 
be expected. The greatest care should be given to keeping the wound 
clean and free of pus. Tight packing of the wound cavity should be avoided. 
The facial muscles should be regularly massaged to forestall or combat 
muscular atrophy. For the same purpose the faradic current should be 
used daily or at least on alternate days. Strychnine sulphate, in doses 
of gr. 1/60 three times a day, and continued over a considerable period, 
is advised, but whether it actually influences the lesion is open to question. 
These measures should be persisted in, and it is usually necessary gradu¬ 
ally to acquaint the patient with the fact that several months may elapse 
before the earliest signs of returning function will be noticeable. 

Before leaving the subject, a word should be said as to the duty of the 
surgeon who is obliged to face the responsibility of a case upon which he 
has operated and in which he is convinced that he has actually divided 
the nerve. In the first place, should the nerve be divided during an opera¬ 
tion and the accident be recognized at the time of its occurrence, there 
would seem to be every reason for attempting at once or within a few days 
of the injury to reunite the segments within the tympanic cavity. Pre¬ 
sumably in most cases the injury occurs at some distance from the genicu¬ 
late ganglion, and I can see no reason why the Fallopian canal should 
not be carefully followed and opened in both directions,— i.e., backward 
toward the bend and then along the descending portion,—and also in the 
opposite direction,— i.e., forward toward its point of entrance into the 
tympanic cavity. With bright illumination, an enlarged radical cavity, 
and with patient, careful work, I can see no reason why it should not be 


FACIO-HYPOGLOSSAL ANASTOMOSIS 


511 


perfectly practicable to take up the divided segments of the nerve within 
the tympanic cavity and reunite them with a suture of fine silk. 

When the knowledge that the nerve has been actually divided or per¬ 
manently injured comes to the surgeon only through the lapse of time and 
absence of any signs of returning function, the question of re-establishing 
function by joining the degenerated peripheral end of the facial to an 
intact cranial nerve (hypoglossal or spinal accessory) must be considered. 

While the results of such attempts in the case of the facial nerve have 
been by no means uniformly successful yet I am of the opinion that, when 
recovery is otherwise hopeless, the operation should be undertaken^ with 
the view to obtaining as much restoration of function as possible, and, 
even should this prove disappointing, to securing sufficient regeneration 
to prevent extreme muscular atrophy. 

Of the two cranial nerves usually considered,— i.e., the hypoglossal 
and the spinal accessory,—the former is the more favorable, for the fol¬ 
lowing reasons: The spinal accessory is the motor nerve of the steVno- 
mastoid and trapezius muscles; when a successful anastomosis between it 
and the peripheral segment of the facial has been accomplished, voluntary 
movements of the shoulder are accompanied by involuntary facial twitch¬ 
ing, while voluntary movements of the face are associated witb involun- 
tary shoulder movements. 

The writer believes that, from the viewpoint of safety, the operation for 
facio-hypoglossal anastomosis belongs neither to the aural surgeon nor the 
average general surgeon. Rather it should be enti usted to the man in any 
community or section who by animal experimentation, special anatomical 
study, dissection work, etc., and by the average results of such operations as 
have come to him, has established Ins special fitness for this peculiarly del¬ 
icate work. On the other hand, conditions are easily conceivable— e.g., in 
regions remote from the large medical centres—in which such cases must 
be operated upon by competent surgeons without this special training, or 
not at all. We, therefore, include a brief outline of the surgical steps for 
uniting the peripheral segment of the facial to the trunk of the hypoglossal. 

The incision for exposing the facial nerve begins at the anterior border 
of the mastoid process and is continued along the anterior margin of the 
sterno-mastoid muscle to a length of about two niches. This incision, winch 
successively divides all the tissues down to the deep cervical fascia, should be 
made with the greatest care not to injure the parotid gland. When the 
deep facia has been reached, a finger introduced into the depth of the wound 
will easily locate in its upper part and in a position corresponding to a point 
just in front of the mastoid tip, a surgical landmark of practical im¬ 
portance, i.e., the styloid process. Around this process the facial trunk 
turns and in this situation it can be felt as a cord-liTe structure rolling be¬ 
tween the process and finger (Taylor). From this point, it passes forward 
to enter the parotid. It is infinitely safer to locate the nerve thus as it crosses 
the styloid process than to look for it at its point of entrance into the parotid 
canal. Having determined by palpation its position and direction, it 



512 


FACIAL PARALYSIS 


should be exposed by dividing the overlying tissues in a direction parallel 
to its course. To attempt to locate it by the sense of sight through a grad¬ 
ually deepening incision running cross-wise to the nerve trunk is almost cer¬ 
tainly to divide it. Once exposed and freed, it should be traced backward 
and then upward toward the stylo-mastoid foramen. The mastoid tip, if 
present and obstructing the way, should be removed. The nerve is then fol¬ 
lowed to its point of exit from the skull, and divided at the highest point 
within the stylo-mastoid foramen that a small, sharp,angular knife will reach. 

The second step of the operation is the more difficult one of isolating the 
hypoglossal nerve. The first surgical landmark is located by palpation, 
as a smooth prominence representing the transverse process of the atlas. 
Two structures to be looked for in order to avoid their injury are the occip¬ 
ital artery and the spinal accessory nerve. The artery is occasionally 
encountered passing upward and outward across the transverse process of 
the atlas, and should be either retracted or divided between ligatures in 
the interest of a clear surgical field. The spinal accessory, also passing over 
the same process, sometimes in front of and sometimes behind the internal 
jugular vein, should also be borne in mind and retracted to a position of 
safety. Both of these structures, as also the internal jugular vein, are cov¬ 
ered by a layer of deep fascia, which should be carefully divided by an 
incision beginning over the transverse process, and then extended in both 
directions to a total length of about IV 2 inches. This incision exposes the 
internal jugular vein, which should be carefully freed by blunt dissection 
posteriorly to permit of its being gently retracted forward. This retraction 
is mechanically equivalent to its rotation forward and should bring into 
view the two characteristic cord-like structures of the hypoglossal and 
vagus nerves, which in their normal relation in this location lie between and 
rather behind the internal jugular vein and internal carotid artery. Usually 
the hypoglossal is the more superficial of the two. It may be identified by 
mechanical stimulation which should cause twitching or contraction of 
its appropriate muscles (styloglossus, hyoglossus, geniohyoid, geniohyoglos- 
sus, thyrohyoid, sternothyroid, sternohyoid), or, perhaps better, it may be 
traced downward to the point where it gives off the descendens noni, and 
bends forward, crossing the occipital and external carotid arteries to pass to 
its distribution In the tongue. Having isolated and surely identified the 
nerve, it should be divided, if an end-to-end anastomosis is contemplated, 
at a sufficiently distal point to allow of its easy approximation— i.e., with¬ 
out tension—to the peripheral segment of the facial. The nerves are held 
together in end-to-end apposition by sutures of fine silk passing only 
through their neural sheaths. The wound surfaces are allowed to come to¬ 
gether and sutured. 

Di*. Alfred S. Taylor, 1 whose paper on the surgical treatment of facial 
paralysis was published as long ago as 1904, and who possibly has operated 
upon more of these cases than any other man in New York, prefers not to 

1 Taylor: Surgical treatment of the facial palsy, with technique or facio-1 ivpoglossal 
anastomosis: Medical Record, February 27, 1904. 








t 





Fig. 300.—Anastomosis of facial and hypoglossal 
nerves. A, Distal segment of facial nerve. B, 
Longitudinal slit in trunk of hypoglossal. C, Im¬ 
plantation of facial in hypoglossal trunk (Taylor). 



FACIO-HYPOGLOSSAL ANASTOMOSIS 


513 


join the facial and hypoglossal nerves in end-to-end anastomosis, but rather 
to implant the end of the divided facial laterally into a longitudinal slit in 
the hypoglossal nerve trunk. The advantage claimed for this operation is 
the fact that paralysis and atrophy of the muscles supplied by the hypoglos¬ 
sal are obviated. 

There has, I believe, been a very considerable diversity of opinion as to 
the relative value of end-to-end anastomosis of two divided nerves, and 
lateral implantation. Certain authors of repute have gone so far as to state 
that lateral implantation should never be employed. Such sweeping 
statements and condemnations are unfortunate in the errors to which they 
occasionally give rise. The only valid argument which could be brought 
against lateral implantation in the case of the facial and hypoglassal nerves 
would be the fact that in actual experience the desired regenerative proc¬ 
esses were not induced; but since the average results have been excellent, 
this argument does not here apply. Surely, unless some very definite gain can 
be assured, the actual division of any of the cranial nerves should be avoided. 

1 am indebted to Doctor Taylor for permission to use the accompanying 
illustrations (Figs. 298, 299 and 300). 

Those who have witnessed his technic and the comparative ease and 
freedom from avoidable traumatism which his skill and experience bring to 
this work, will the more readily agree with my contention that these cases 
should be entrusted only to those whose special training best fits them to ac¬ 
complish the mechanical and physiological results which are the ends in view. 

Even when the mechanical work of this operation has been success¬ 
fully executed, both surgeon and patient must be prepared for a consider¬ 
able lapse of time before any evidences of returning function will be 
noticeable. Bowlby, 2 than whom perhaps no man has had a larger experi¬ 
ence in the surgical treatment of injured and degenerated nerves, has this 
to say in regard to the interval which in cases of long-standing degenera¬ 
tion must be allowed for between the neurorrhaphy and the reestablish¬ 
ment of function: “What most interested me was to find that in many 
patients who had completely recovered, there had been a long period of 
many months, or even years, between the time of injury and the return 
of sensation or motion, and I saw that no case should be written down as 
a failure simply because the operation of suture was not followed by im¬ 
mediate success. ... If there is one fact more than another which 
stands out in the clinical histories of the patients who have been under 
my own observation, it is that, after the failure of union by first intention, 
after trophic changes of many kinds, after complete atrophy and degener¬ 
ation of the paralyzed muscles, recovery may yet be complete.” 

2 Bowlby, Anthony A.: Injuries and Diseases of Nerves and their Surgical Treat¬ 
ment, Blakiston, Phila., p. 155. 


33 




CHAPTER XX. 

CONGENITAL ABNORMALITIES OF THE AURICLE. 

The anatomical defects, or abnormalities, of the auricle are so varied 
as almost to defy concise classification. Within certain limits, considerable 
departures from the normal standard either as to size or shape may attract 
comparatively little notice so long as the two ears are alike. On the other 
hand, a very slight unilateral abnormality may constitute a noticeable 
deformity. For example, few simple defects attract the gaze more insis¬ 
tently than asymmetry in position,— e.g., one auricle standing more prom¬ 
inently from the side of the head than its fellow. Again, different parts 
of the auricle vary in the extent to which any anatomical variation en¬ 
gages the eye. Thus, very considerable changes in the arrangement of 
the cartilaginous folds may pass unnoticed, while even moderate variation 
in the size or shape of the lobule will attract the gaze unpleasantly and 
must therefore be considered a deformity. As to the variations in size— 
the auricles being normal in contour and position—a small ear is usually 
accounted beautiful, while any enlargement above the normal standard 
is unattractive and therefore popularly accounted a defect. 

Among the recognized types of aural deformity may be mentioned the 
following: 

I. Macrotia, a term used to describe anatomical conditions result¬ 
ing in abnormal increase in the size of the auricle. The increase in size 
may be due to uniform or symmetrical enlargement of all its parts or, as is 
more frequently the case, may be due to redundancy of that portion of the 
auricular cartilaginous plate situated between the margin of the concha and 
the margin of the helix. If, to offset this, the peripheral margin is deeply in¬ 
folded, the general outline of the ear may not be greatly enlarged, but there 
is produced the disfiguring anomaly described as the “redundant helix” 
(Fig. 301). When this deep infolding of the helix does not occur, the pro¬ 
longation of the auricular plate—even though it be extended in the normal 
plane—increases noticeably the distance between the peripheral margin, or 
helix, and the side of the head, giving the effect of abnormal protrusion 
(Fig. 302). When the upper part of the auricular plate is narrowed and 
prolonged upward so as to represent a point instead of the usual curve, 
the peculiar type known as a “satyr’s ear” is produced (Fig. 303). 

Redundancy of the lobule may form part of a uniform enlargement or 
may occur independently. It produces a conspicuous abnormality, which, 
fortunately, is easily corrected. 

II. Polyotia, or the occurrence of supernumerary auricles, is, fortu¬ 
nately, a rare condition, of which, however, authentic cases have been 
recorded. 

III. Supernumerary Parts.- —Of much more frequent occurrence 
is the condition in which there are supernumerary parts, usually small 

514 



SUPERNUMERARY PARTS 


515 


cartilaginous nodules covered with normal skin and closely appended to 
the auricle. Their most usual position is immediately in front of or below 
the tragus, or below the inferior auricular fold,— i.e., beneath and below 



Figs. 301, 302, 303.—Three common types of macrotia. 



Fig. 304 .—Supernumerary cartilaginous Fig. 305.—Supernumerary nodules, 

nodules. 


the lobule. This congenital abnormality is not very unusual,—several 
cases being seen yearly in any large clinic, and is usually associated with 
an otherwise normal auricle (Figs. 304 and 305). 



516 CONGENITAL ABNORMALITIES OF THE AURICLE 

IV. Projecting Auricle, “Lop Ear” (Fig. 306).—This condition is 
usually symmetrical,— i.e., involves equally the two ears. In some cases 
it is apparently clue to a redundancy of the entire cartilaginous plate irom 

the margins of the cartilaginous meatus upward and backward to the 

helix. As*a consequence, the- carti¬ 
lage is curled outward or forward as 
well as enlarged. Occasionally with 
this condition there is in one or both 
ears an obliteration of the normal 
bend or fold of the antihelix, which 
increases greatly the deformity by 
throwing the auricle still further 
forward and downward. In another 
class of projecting ears the displace¬ 
ment is apparently due to a deepen¬ 
ing of the cavity of the concha, this 
giving rise to a prominent hemisphe¬ 
rical projection on the posterior sur¬ 
face of the auricle which throws the 
ear forward. 

In all the above conditions the ears 
may be and usually are functionally 
normal, or at least there is no func¬ 
tional impairment dependent upon 
the auricular abnormality. The treatment is, therefore, undertaken solely 
for the purpose of relieving deformity or improving personal appearance. 
This, however, is no reason for regarding this field of work as not worthy 
of special study. 

V. Microtia. —A class of deformities coming under a wholly differ¬ 
ent category from any of the above are those grouped under the general 
term microtia. Meaning literally abnormal reduction of the size of the 
ear, it usually describes anomalies of form so gross that all resemblance to 
the normal auricle is lost. Moreover, it generally includes malformation 
or absence of the auditory canal, and frequently changes in the tympanic 
or even in the labyrinthine structures. Microtia is usually associated, 
therefore, with serious loss of hearing. In some cases not only the mem- 
brano-cartilaginous meatus but also the osseous meatus is completely 
absent. As microtia is very often bilateral, many of its unfortunate 
victims are practically deaf-mutes. As to the auricular deformity, it in¬ 
cludes a variety of conditions from a shrivelled and misshaped roll of 
cartilage to a keloid-like band of skin-covered cartilage with complete 
absence of auditory meatus (Figs. 307 and 308). 

From the viewpoint of the deformity, the possibilities of treatment may 
be dealt with briefly. In a majority of cases the auricular cartilage is so 
rudimentary or the malformation so gross that by no wizardry of plastic 
surgery could any semblance to a normal auricle be produced. But there is 








MICROTIA 


517 


a more important side to the question of treatment,— i.e., the possibility of 
surgical measures for the improvement or more often the establishment of 
hearing. Any discussion of this question must take the form of a discussion 
of the various observations and theories as to the morbid changes usually 
present. Does a grossly malformed auricle with deafnesss usually or always 
indicate a coincident defect of the auditory labyrinth? Does congenital 
atresia of the auditory canal necessarily imply a defective perceptive 
mechanism? Should all cases of bilateral congenital atresia be operated 
upon with a view of establishing or improving the auditory function? 




Fig. 307.—Microtia. 


Fig. 308.—Microtia. 


Theoretically, since the labyrinth is developed from the cartilaginous 
skeleton, and the structures of the conducting mechanism are of distinctly 
later developement from its enveloping membranes, it is difficult to under¬ 
stand why any congenital defect may not exist in either mechanism in¬ 
dependently of the other. But whatever one’s personal theory, if one 
examines the literature bearing on these abnormalities, one finds such di¬ 
versity of opinion, that one is forced to conclude that many aspects of the 
subject are still sub judice. 

The comparatively small number of published reports of cases oper¬ 
ated upon by American surgeons leads one to suspect that the results as a 
rule have not been particularly gratifying. Dr. John R. Rage’s case 1 of 
congenital bilateral microtia with atresia of the canals is interesting and 


1 Page, J. R.: Congenital bilateral microtia, etc. Transactions Amer. Oto. Soc. 1914. 






518 


CONGENITAL ABNORMALITIES OF AURICLE 


instructive in that the anatomical defects revealed by the operation and the 
surgical method pursued are clearly stated. While the results of hearing 
tests before and after operation are not given in detail, it is clear that the 
hearing was greatly improved. But analysis of the operative findings in this 
case, with the normal caloric reactions and prompt improvement of hear¬ 
ing, shows that the deafness was due to defective sound transmission rather 
than to a defective labyrinth. Too great optimism as to the average results 
of surgical intervention would not, therefore, be justified as a logical deduc¬ 
tion from this case. 

In this country, probably the most comprehensive monograph on this 
subject is that published in 1917 by Dr. Lee Wallace Dean 2 of Iowa City. 
This paper includes interesting and extensive references to the literature 
of the subject with in some cases brief synopses of case reports and the de¬ 
ductions based thereon. Dr. Dean ends his paper with an instructive and 
unusually complete history of a case from his own practice. This case has 
so clear a bearing on one mooted point in the interpretation of these con¬ 
genital defects, that the salient facts will be briefly stated. 

The history is that of a boy of 15 years, with auricles of normal size and 
shape but with complete atresea of both canals. Hearing “poor since 
birth” and rapidly failing. Hearing defects typical of a disturbance of 
sound conduction. Operation demonstrated in each ear a movable incus 
and stapes; no malleus discovered; no annulus or drum membrane. The 
normal space of the bony meatus was occupied on each side by solid bone. 
In the effort to establish a practical sound-conducting apparatus this bone 
was drilled out by an electric burr. To provide an orifice for the artificial 
canal thus formed a large opening was made in the concha. The canal and 
small aditus to which it led was later lined with Thiersch grafts, resulting 
ultimately in complete dermatization. As a result of the operation, which 
was practically the same on the two sides, the hearing was immensely im¬ 
proved. Hearing distance for conversational voice increased from 3 feet 
and 5 feet (right and left) to 48 feet. The case is of great importance in 
demonstrating that atresia of the canals may coexist with perfectly normal 
labyrinths, and as suggesting that the prognostic value of operative inter¬ 
vention is probably in direct ratio to the amount of hearing before operation. 

Apparently one is justified at least in the following conclusions: (1) 
Bilateral microtia with congenital atresia of the canals and accompanied by 
extreme deafness— i.e., deafness so pronounced as to render the acquisition 
of speech doubtful—offers so little definite promise of improvement by any 
means at our disposal as to make operative intervention of questionable 
prognostic value. Naturally, in the first 2 or 3 years of life, hearing tests 
are not very reliable, and one may have to assume risks in operating, as the 


2 Dean. L. W.: Report of a case of bilateral, congenital osseous atresia of the auditory 
canals: Transactions American Laryngological, Rhinological and Otological Society 
1917. 





MICROTIA 


519 


only hopeful possibility. Clearly only one ear should be operated at a 
time. (2) Bilateral microtia or atresia of the canals (or both) with hear¬ 
ing; in either ear of sufficient acuteness to suggest an intact or at least 
functionally useful perceptive mechanism, should be operated upon. 

In operative cases, the rational procedure is to open the antrum from 
behind as for a radical operation, and lower the posterior canal wall, if a 
canal exists. In the absence of a bony meatus the tympanum should be 
exposed by very careful removal of the outer wall of the aditus. In the 
absence of a drum membrane the malleus and incus, if present, should be 
removed. A bony meatus may then be made, if conditions permit, by re¬ 
moval of bone from within outward. The plastic work for providing a 
suitable orifice and canal would of course have to depend upon the anatom- 



Fig. 309. Fig. 310. Jig. 311. 

Figs. 309, 310, 311.— Usual method of reducing an abnormally large auricle (Goldstein). 


ical condition of each individual case. The electric burr may possibly 
play a useful role in these cases, and skin grafting will in all cases be an 
essential means of maintaining the artificial orifice and meatus. 

The treatment of the lesser aural abnormalities is almost wholly 
surgical. When it is observed that the ears of an infant or very young 
child, while of normal size and shape, tend to stand out prominently from 
the side of the head, something may be done to correct or avert the de¬ 
formity by bandaging the ears to the side of the head at night, the use of 
nightcaps, etc. Such appliances, however, are uncomfortable, not con¬ 
ducive to sound sleep, and the results are extremely uncertain. We 
shall consider, therefore, only the surgical treatment ol patients who shall 
have reached an age at which palliative measures are obviously useless. 

When the abnormality is chiefly that of unusual size,— i.e., depends 
mainly upon undue peripheral growth or expansion of the cartilaginous 




520 


CONGENITAL ABNORMALITIES OF AURICLE 


frame,—the deformity may usually be made less conspicuous by an opera¬ 
tion fixating the auricle more closely to the side of the head. This in 
competent hands is a safe procedure,— i.e., not likely to result in peri¬ 
chondritis. Actual reduction of size, on the other hand, can be obtained 
only as the result of an operation including some removal of cartilage. 
An operation described by Dr. Goldstein, 3 designed to reduce the vertical 
diameter of an abnormally long auricle, is clearly shown in the accompany¬ 
ing figures (309, 310, 311). 

After the horizontal incision ci-b (Fig. 309) is made, the upper segment 
is overlapped upon the lower and drawn down until the desired reduction 
in size is attained. The redundant wedge-shaped segment of cartilage is 
then removed by a careful incision through the line b-c, Fig. 310. If the 
peripheral edges do not meet,— i.e., do not form a continuous peripheral 
margin,—they may be brought into proper line by removal of a second 
small wedge of tissue from whichever segment extends beyond the other,— 
e.g., the portion included in the triangle n-f-z, Fig. 311. This, however, 
should usually be avoided. The parts are then united by a line of in¬ 
terrupted silk sutures passing through the cartilage and both skin surfaces 
and tied on either the posterior or anterior surface of the auricle. 

For displacement due to abnormal width of the auricular cartilage, 
Goldstein has devised an ingenious operation (Figs. 312, 313, 314, 315), 
for which we append his own description: “The curvilinear incision a-b 
(Fig. 312) is made on the posterior surface of the auricle, almost corre¬ 
sponding with the natural ridge of the antihelix anteriorly. The convexity 
of this curved incision line presents outward toward the rim of the helix. 
The flap is shaped so that, when it is dissected upward and over toward 
the mastoid area, the largest possible surface of cartilage is exposed. The 
dissection of the integument flap and perichondrium from the cartilage is 
simple, and, as the adhesion of the perichondrium is not firm, it can be 
quickly done. 

“When the cartilage is cleanly exposed, an incision in the line e-f 
(Fig. 313), curving inward, almost at a right angle at points e and /, is 
made through the cartilage, care being taken not to wound the underly¬ 
ing integument which forms the anterior covering of the auricle. With a 
narrow, blunt elevator, such as is used in the resection of the nasal septum, 
the two cartilaginous flaps at c-d and e-f are now carefully elevated from 
the underlying perichondrium to a sufficient breadth to admit of their 
manipulation, and to permit the flap at c-d to be superimposed upon the 
flap at e-f, when brought together by a series of two mattress sutures, 
each suture being passed twice through each of the cartilages. When 
gentle traction is applied in tightening the sutures, the two cartilaginous 
flaps will be drawn over each other and the width of the auricle reduced 
in the same proportion as the sutures are introduced from the edges of 
the respective cartilaginous flaps. The sutures are applied by first passing 


3 Goldstein, M. A.: The Laryngoscope, vol. xviii, No. 10, pp. 835-7. 






Fig. 312. 


Fig. 313. 






Fig. 314. 

Figs. 312, 313, 314, 315.—Operation for reducing abnormally 


Fig. 315. 

wide auricle. (After Goldstein.) 




<0 QJ 









TREATMENT OF PROJECTING EARS 


521 


a sharply-curved needle, armed with thin chromatized catgut, through a 
point at the upper end of flap c-d, then downward through flap e-f, then 
over and under through an opposite point in flap c-d. 

“Another suture is similarly placed in the lower part of these flaps. 
The cartilage is tough and will stand considerable traction when the 
sutures are brought together. The sutures are then tied over flap c-d 
(Fig. 314), the redundancy at the edge of the integument flap a-b is then 
carefully cut away and the integument stitched in position in the original 
line of incision (Fig. 315). With the traction produced by the overlap¬ 
ping of the cartilaginous flaps, some slight wrinkling or puckering may at 
first appear on the anterior surface of the auricle, but if the anterior peri¬ 
chondrium and integument have been liberally elevated from the cartilage, 
this wrinkling of the integument will disappear with the healing of the 
wound.” 

In any operation involving incision or removal of auricular cartilage, 
the chances of failure are considerable. In the first place, one difficulty 
is the cosmetic necessity of obtaining the same mechanical result in each 
ear. Healing by first intention is essential to a perfect result. Should 
infection occur, perichondritis may result. This in turn may lead to in¬ 
flammation and finally necrosis of the cartilage itself, with resulting deform¬ 
ity far greater than that which the operation was designed to correct. 

There are, of course, other operations than the two above mentioned 
for reducing the size of a large auricle, but, as a rule, they are more com¬ 
plicated, call for multiple incisions of the cartilage, .and the chances of 
infection and perichondritis are proportionately greater. 

Removal of Supernumerary Nodules. —The correction of the dis¬ 
figurement caused by the presence of supernumerary parts or appendages 
(Figs. 304, 305) consists in their surgical removal. The overlying skin 
is carefully dissected up, and the cartilaginous nodules or projections 
forming the basis of the deformity are excised. The skin flaps are then 
brought together, redundant portions removed, and the wound closed 
with silkworm-gut sutures. 

Treatment of Prominent or Projecting Ears. —In those cases in 
which the auricle is neither malformed nor abnormally large, and in which 
displacement is mainly forward, the condition may be corrected by the 
comparatively simple operation indicated by Figs. 316, 317, and 318. 

With tooth thumb forceps the skin is caught up at a point upon the 
posterior surface of the concha a variable distance from the postauricular 
fold, and by this the auricle is drawn backward and inward against the cor¬ 
responding mastoid surface. If this brings the auricle into an approximately 
normal position, the point grasped by the forceps and that upon the mas¬ 
toid surface with which it comes in contact are nicked (Fig. 316, x, x). 
These coming together represent the common point for fixating the auricle 
to the side of the skull. A curved line is now marked on the posterior sur¬ 
face of the concha, joining the two ends of which a similar line is marked 
upon the skin covering the mastoid (Fig. 317). In each case these lines 


522 


CONGENITAL ABNORMALITIES OF AURICLE 


traverse the contact points (x). We have thus marked out upon the post- 
auricular surfaces of the auricle and mastoid an area from which the skin 
and soft parts are to be dissected up and removed. Upon the auricular sur¬ 
face the tissues are dissected from the perichondrium and upon the mastoid 
from the periosteum. In other words, neither the cartilage nor the bone 
is deprived of its nutritive and protective membrane. When the auricle 
is now pushed back into normal position, we have a raw surface upon the 
back of the auricle in contact with a raw surface of similar shape upon the 
mastoid. The parts are held in apposition by sutures uniting the skin 



Figs. 316, 317, 318.—Operation for the correction of moderate projection. 


edges forming the boundaries of the two denuded areas (Fig. 318). Both 
ears should be operated upon at the same time. Following the operation, 
a large pad of sterile gauze is placed over each ear, and a bandage applied. 
At the end of five or six days when the stitches are removed, the auri¬ 
cles are fixated in their new and more correct position by the skin suture 
line and by the firm adhesion of the broad surfaces from which the skin 
was removed. 

Ruttin’s Operation. —Ruttin’s operation, involving practically the same 
principles as those applied in the preceding, is appropriate to cases of more 
exaggerated displacement, and is proportionately more radical. The 
essential features are graphically shown in the accompanying illustrations 
(Figs. 319 to 323). 

The auricle is forcibly placed against the side of the head (Fig. 319), 
and a line is marked upon the postauricular surface corresponding to the 
centre of the posterior limit of auricular contact (Fig. 319). This line is 
then made curvilinear and parallel with the postauricular fold, or line of 
postauricular attachment (Fig. 320). A similar curvilinear incision is 
next made upon the posterior surface of the auricle just behind the line 
of auricular attachment, and a curved flap dissected up from the perichon¬ 
drium (Fig. 321). The upper and lower extremities of the two incisions 
are now united by horizontal incisions, and the included soft parts dis- 



DUEL’S OPERATION FOR PROJECTING EARS 


523 


sected up and removed (Fig. 322). The curved auricular flap is finally 
drawn backward, carrying the auricle with it, and sutured to the corre¬ 
sponding margin of skin behind the ear (Fig. 323). The ear is held against 
the side of the head by a pressure pad and bandage. When healing is 
complete and the stitches are removed, the auricle is held in the new and 
less conspicuous position by the suture line and by the adhesion of the 
broad surfaces denuded in the operation. 




Fig. 322. Fig. 323. 


Figs. 319, 320, 321, 322, 323.—Ruttin’s operation for projecting auricles. 


This operation is practical, and its results should be permanent. A 
possible disadvantage is the obliteration of the space between auricle and 
scalp behind the ear. 

Duel’s Operation. —Duel’s operation is an effort to correct a forward 
and outward displacement of the auricle without obliteration of the post- 
auricular fold or sulcus. 

By means of two thumb forceps the skin covering the posterior surface 
of the auricle is caught up at two points (Fig. 324, x, x), by which the 
auricle is drawn inward against the side of the head. The skin points 
caught by the forceps are brought into contact with the side of the head 
-along a more or less vertical line a little behind the postauricular fold. 








524 


CONGENITAL ABNORMALITIES OF AURICLE 


Different points upon the posterior surface of the pinna are tried until two 
are found which, when brought into appropriate contact with the side of 
the head near the attachment of the auricle, maintain the auricle in proper 
position. These contact points are then marked,—those on the posterior 
surface of the pinna being pinched with the forceps, while those behind 
the ear are nicked. The four contact points thus marked are united by 
three incisions, two horizontal and one vertical (Fig. 324), thus outlining 
a quadrilateral flap which must be dissected up as indicated in Fig. 325. 
About a half inch behind and parallel with the first vertical incision, a 



Fig. 327. , Fig. 328. 

Figs. 324, 325, 326, 327, 328.—Duel’s operation for projecting ears. 


second incision is made outlining between them a narrow strip, which, 
when dissected from the underlying bone, forms a movable band attached 
only above and below (Fig. 325). Beneath this band the quadrilateral 
flap is now introduced, and, when rather forcibly drawn back, as shown 
in Fig. 326, increases the auricular bend at the antihelix and draws the 
auricle into position against the side of the head. When the deformity is 
caused by the absence of the usual bend of the antihelix, this strapping of 
the ear inward is designed to create such a bend by folding the auricular 
plate upon itself. Having drawn the quadrilateral flap beneath the ver- 

























DUEL’S OPERATION FOR PROJECTING EARS 


525 


tical band and well backward, we have the middle third of the flap hidden 
beneath the vertical band, and the posterior third extending well behind 
it as in Fig. 326. The next step is to mark out upon the postauricular 
surface the narrow quadrilateral area lying beneath the posterior end of 
the flap, throughout which the skin and soft parts must be removed. 
The skin must also be removed from the middle third of the flap,— i.e., 
that part of it which is destined in the completed operation to lie under 
the vertical band. These steps completed are shown in Fig. 327. The flap 
is now again drawn under the vertical band until the denuded area is in 
contact with the under surface of the latter, and is then secured in position 
by the three vertical rows of interrupted sutures shown in Fig. 328. For 
this operation sutures of fine silk are the best. During all these manipula¬ 
tions the vertical band must be held in position by an assistant; and after 
the final sutures are placed, a compression pad is necessary to keep the 
various raw surfaces in appropriate apposition and contact. 

Duel’s operation is more complicated, more difficult, and in the hands 
of the average surgeon its results are therefore more uncertain than those 
of the two preceding operations. 


CHAPTER XXI. 

NON-SUPPURATIVE DISEASES OF THE LABYRINTH. 

Meniere’s Disease. —Definition: This term may be properly applied 
only to the condition in which pronounced deafness and the phenomena 
of vestibular irritation occur suddenly as a result of hemorrhage into 
the labyrinth. 

In its true form it is unquestionably one of the rarest of lesions. Meniere 
has given a clear description of the first case observed clinically and com¬ 
ing to autopsy. 1 A young girl, during a menstrual period, was attacked 
with sudden extreme vertigo, nausea and vomiting, loud tinnitus, and 
absolute deafness. Death occurred on the fifth day of the attack. Post¬ 
mortem examination showed the presence in the semicircular canals of a 
thick bloody exudate, only a trace of which could be found in the vesti¬ 
bule, and which was not present in the cochlea. The most careful exami¬ 
nation of the brain and cord failed to reveal any abnormal condition, and 
the exact cause of death was not determined. 

Etiology. —While many conditions—including pronounced anaemia, 
leukaemia, rheumatism, nephritis, intense heat, and prolonged exposure 
to the sun—are mentioned as among the possible causes, cases of the 
disease, typical clinically and verified by autopsy, have not been observed 
in sufficient number to justify any conclusive statements. Politzer men¬ 
tions that cases presenting all the clinical features of the disease have died 
in which the post-mortem findings have failed to provide any evidence of 
hemorrhage into the canals, and, per contra, a hemorrhagic exudate within 
the vestibule and canals has more than once been observed post mortem 
in cases in which no history of typical Meniere’s symptoms during life 
could be obtained. Furthermore, Meniere’s case, upon which our con¬ 
ception of the disease still very largely rests, does not supply a logically 
complete picture; for one of the conspicuous clinical features of the attack 
was the sudden and profound deafness, yet his post-mortem examination 
revealed no abnormality within the cochlea. 

In considering this lesion as a pathologic entity, it must be remembered 
that many conditions which we now know to be capable of inducing 
identically the same clinical phenomena were practically unrecognized 
until a comparatively recent date. It is probable, therefore, that many 
cases have in the past been recorded as true examples of Meniere’s disease 
which have in reality been the result of other conditions, the nature 
of which would now be easily recognized. The disease is still more or 
less wrapped in mystery, which future investigations may serve to clear up. 

Diagnosis. —According to our present concept of the disease, the 


1 Meniere: Gazette medicate de Paris, 1861, p. 598. 
526 



MENIERE’S DISEASE 


527 


diagnosis depends not only upon the clinical features of the attack, but 
demands also a knowledge of the condition of the patient’s ears before 
and immediately following the attack. To justify a reasonably positive 
diagnosis, the attack must occur in an individual whose ears are known 
previously to have been normal or approximately so, and inspection of the 
ears shortly after the onset must show absence of any pathologic changes 
within the tympanum upon which an hypothesis of possible labyrinthine 
infection might be based. 

The symptoms are those characteristic of sudden, intense irritation of 
the vestibular apparatus plus ablation of the cochlear function. The 
attack begins with severe subjective vertigo, great disturbance of static 
equilibrium, loud tinnitus, nausea and vomiting, and pronounced deaf¬ 
ness in one or both ears. The patient does not, as a rule, lose conscious¬ 
ness. At the onset he is forced by the urgency of the symptoms to go to 
bed. Sudden movements of the head or the attempt to rise aggravate the 
subjective symptoms and may induce vomiting. Nystagmus without 
doubt is an invariable phenomenon of the onset. 

As with every disorder depending upon an organic lesion, the severity 
of the symptoms varies with the extent and character of the lesion. It is 
conceivable that very slight hemorrhage, confined to one or more of the 
canals, might induce very pronounced and distressing symptoms, which, 
however, might disappear with the final absorption of the exudate. Only 
in this way can be explained certain very typical recorded cases in which 
recovery has been fairly rapid and apparently complete. 

A form of the disease described in most text-books under the term 
“apoplectic form of Meniere’s disease” is characterized by a similar train 
of clinical phenomena plus symptoms of cerebral disturbance, the chief 
of which being loss of consciousness. The loss of consciousness follows 
closely upon the onset and is of short duration, leaving the patient at 
first in a condition bordering upon collapse, from which he gradually 
recovers. The exact pathologic basis of such seizures is as yet altogether 
hypothetical. It is possible that they may eventually be proved to be 
quite unrelated pathologically to true Meniere’s disease. 

The prognosis depends on the extent of the lesion. It is conceivable 
that a very slight extravasation of blood might be absorbed, leaving little 
or no disturbance of function. On the other hand, the membranous laby¬ 
rinth is known to be a structure so extremely sensitive to any form of direct 
mechanical injury that it is difficult to believe that a considerable bloody 
exudate could fill any of the bony compartments of the labyrinth without 
causing practical destruction, or at least permanent ablation of function, 
of the membranous structures contained therein. It is one of the incon¬ 
sistencies of our conception of the disease that, while the semicircular 
canals are looked upon as the characteristic site of the lesion, permanent 
deafness is said in severe cases to be one of the most constant and char¬ 
acteristic sequelae. ...... 

Treatment. —The logical treatment is that of any irritative lesion of 


528 


NON-SUPPURATIVE DISEASES OF LABYRINTH 


the labyrinth plus measures appropriate to any form of concealed hemor¬ 
rhage. Absolute rest in bed should be enforced during the first two or 
three days of the attack. It might be well, unless uncomfortable to the 
patient, to have the head slightly raised. A laxative should be adminis¬ 
tered and particular attention directed to keeping the bowels freely moved. 
During the first twenty-four or forty-eight hours fluid diet is indicated. 
Applications of dry heat to the feet, calves of the legs, and abdomen, and 
cold to the head have been advised, probably on the hypothesis of a path¬ 
ologic analogy between the lesion and cerebral hemorrhage. They prob¬ 
ably are without influence either upon the lesions or the resultant symptoms. 

For the various drugs advised I can see no indication, unless it be the 
iodide of potassium, small doses of which, after the acute stage of the 
attack has passed, may tend to promote absorption of the fibrinous exu¬ 
date which is the pathologic basis of the disease. 

“ Vertigo ab aure laeso.” —A term which time-honored custom has 
transmitted from one text-book to another, but which in the author’s 
opinion should long since have been dropped from otological literature 
and parlance, is “vertigo ab aure laeso.” It is applied to the short attacks 
of intense vertigo, ataxia, tinnitus aurium, and vomiting which occur as 
a rare accompaniment of cases of otosclerosis or chronic hyperplastic 
otitis media, and which have been supposed to be in some way related to 
mechanically induced changes in intra-labyrinthine pressure. A careful 
analysis of the symptoms described shows that they coincide exactly with 
the usual phenomena of vestibular irritation, the one characteristic fea¬ 
ture not invariably mentioned being nystagmus. In the light of recent 
advances in our knowledge, a close study of the symptoms will show these 
attacks to depend upon causes not easily traceable to a tympanic lesion, 
or at least to accord better with other theories of origin. The writer does 
not wish to belittle the value of the clinical observations recorded under 
this name, but simply to protest against the retention of a term which 
our advancing knowledge of labyrinthine phenomena should have rendered 
obsolete. These cases present perfectly characteristic manifestations 
either of direct irritation of one or both labyrinths, or of the excitation 
of one labyrinth as a result of sudden paralysis or ablation of function of 
the opposite organ. Each case should be subjected to the most careful 
observation and study, and an attempt made to determine exactly the 
underlying cause. “Vertigo ab aure laeso” is an inexact term which has 
supplied a convenient cloak for a gap in our knowledge. 

Leukaemic Deafness. —The so-called leukaemic deafness is the result 
of certain morbid changes within the labyrinth which occasionally occur 
in cases of leukaemia. Politzer, who reported the first authentic case of 
leukaemic labyrinthitis in 1885, cites Vidal ,and Isambert as having esti¬ 
mated that the aural lesion occurs in 10 per cent, of all cases of leukaemia. 

The most characteristic pathologic change is the presence of a fibrin¬ 
ous, bloody exudate and masses of lymph-cells in both the perilymph and 
endolymph spaces of the labyrinth. Both the cochlear and vestibular 


ANAEMIA OF THE LABYRINTH 


529 


sections of the labyrinth are usually involved. In Politzer’s case masses 
of “leuksemic plaques consisting of lymph-cells ” were found within the 
scala tympani resting upon the basilar membrane and bony wall of the 
canal. Somewhat similar post-mortem findings have been reported by 
other observers. In England the disease has been studied by Richard 
Lake, who has been able to exhibit a number of characteristic pathological 
specimens of the lesion. 

Symptoms. —Two clinical types of the disease have been recorded: (1) 
Those in which the symptoms were obviously the result of sudden hemor¬ 
rhage into the vestibule and canals, and therefore resembled closely a typi¬ 
cal attack of Meniere’s disease,— i.e., intense vertigo with attendant ataxia, 
loud tinnitus, and deafness; and (2) cases in which hemorrhage has played 
a minor part, the characteristic change being an infiltration of the endosteal 
lining of the bony spaces involved, and the deposition of masses of lymph- 
eells within both the perilymphatic and endolymphatic spaces of the laby¬ 
rinth. Great thickening of the endosteum has been noted in some cases. 
Such a lesion would lead logically to a more gradual and less spectacular 
development of symptoms,— e.g., impairment of hearing of labyrinthine 
type, progressing rapidly to an extreme grade of deafness. Symptoms of 
disturbed vestibular function also characterize this form of the disease, but 
are much less pronounced than in the hemorrhagic type of the lesion. 

Anaemia of the Labyrinth. —It is not always easy to trace with any 
certainty the symptoms due to anaemia of the labyrinth to their source. 
It is known, however, that in cases of profuse traumatic hemorrhage, in 
parturition,—in fact, in any condition causing sudden withdrawal from 
the body of large amounts of blood,—loud tinnitus aurium, intense dizzi¬ 
ness, and in some cases vomiting, are present. In such cases the tinnitus 
and vertigo, and in all probability the vomiting, seem to be clearly of 
vestibular origin, and are explainable upon no other hypothesis than that 
of sudden diminution of the vestibular blood supply. 

The attacks of vertigo and tinnitus which occasionally occur during 
the course of wasting illnesses— e.g., severe typhoid fever—may be due 
either to direct irritation of the vestibular structures by toxic substances 
circulating in the blood or to the participation of the labyrinth in the 
ansemia which is a logical result of the disease. On the other hand, the 
extreme dizziness, particularly if accompanied by loud tinnitus, which 
may attend the first attempt of a convalescent from any wasting disease 
to assume the upright position,— i.e., to stand,—would seem to be the 
logical expression of a sudden diminution of the vestibular arterial supply. 
These are instances of labyrinthine disorder which rapidly correct them¬ 
selves as the patient regains his normal condition. They are cited as 
convincing examples of aural disorders directly depending upon laby¬ 
rinthine anaemia. 

More difficult of positive diagnosis—impossible of correct interpreta¬ 
tion except through a very careful and thorough process of exclusion, but 
of undoubted occurrence—are cases of vertigo with auditory impairment 

34 


530 


NON-SUPPURATIVE DISEASES OF LABYRINTH 


resulting from the severer forms of anaemia. The symptoms are similar 
in kind to those of vestibular irritation through other agencies,— i.e., 
vertigo, marked disturbance of static equilibrium, subjective noises, and 
loss or impairment of hearing. One diagnostic sign of the origin of such 
an attack (Dundas Grant) is said to be the relief of symptoms when the 
patient assumes the recumbent position. Greater dependence, however, 
must be placed upon blood counts and the exclusion of other causes. 

There are two considerations which make it of particular importance 
that cases belonging to this class should be correctly diagnosticated,— 
viz., (1) only a determination of the underlying cause will lead to an effec¬ 
tive plan of treatment, and (2) failure to institute the proper treatment 
may leave the patient in the most favorable condition for the develop¬ 
ment of otosclerosis (H. A. Gray, see pages 249-250). 

Treatment. —The treatment is obviously constitutional rather than 
local. Rest, abstention so far as circumstances may admit from business 
cares and worries, and the administration of constructive tonics are our 
chief aids in relieving such patients. 

Syphilis of the Labyrinth. —Four clinical types of labyrinthine syphilis 
are recognized,—viz., (1) The congenital type, seen in its most character¬ 
istic and easily recognized form in children exhibiting other stigmata of 
the disease. The aural lesion is usually bilateral, though one ear may be, 
and usually is, more seriously impaired than the other. Examination of 
the ears may reveal physically normal drum membranes, or the physical 
signs of middle-ear suppuration may render the syphilitic character of the 
labyrinthine affection less easy to recognize. The deafness is of distinctly 
labyrinth type and usually of advanced grade. Examination of the child 
shows in a certain percentage of cases the characteristic notched condition 
of the teeth (Hutchinson’s). According to Fraser, 2 this defect occurs in 
50 per cent, of cases. Interstitial keratitis is another defect occasionally 
met with, as also are destructive lesions (defects) of the soft and hard 
palate. With or without these defects, the child not infrequently pre¬ 
sents a stunted, prematurely old appearance which is more or less char¬ 
acteristic of these little unfortunates. The above abnormalities mark the 
most pronounced and therefore conspicuous form of congenital syphilis. 
There are many cases, however, in which the child does not exhibit such 
obvious stigmata, in which case a thorough physical examination, a care¬ 
ful analysis of the family history, and resort to the Wassermann test may 
be necessary to establish a correct diagnosis. 

The prognosis, so far as the auditory function is concerned, is hopeless. 

(2) The second variety of syphilitic labyrinthitis is that which occa¬ 
sionally complicates the acquired form of the disease in adults. It develops 
most frequently in the late secondary or in the tertiary stage, rarely in the 
primary stage of the disease. It is characterized clinically by very sudden 
and usually very extreme deafness in one or both ears. That the vestib- 


2 Fraser: Journal of Laryng., Aug., 1909. 




SYPHILIS OF THE LABYRINTH 


531 


ular apparatus is also involved in a very large percentage of cases is shown 
by the frequent evidences of disturbed equilibrium,— e.g., nystagmus, 
vertigo, static ataxia, etc. When the lesion is unilateral and completely 
annuls the function of the affected vestibular mechanism, the onset is 
necessarily characterized by all the usual phenomena of vestibular irritation 
or excitation. When both labyrinths are simultaneously paralyzed, the 
patient exhibits the type of vertigo and ataxia characteristic of vestibular 
paralysis. The writer has recorded the history of such a case, 3 in which the 
patient was absolutely deaf in both ears, and both vestibular mechanisms 
were absolutely non-irritable by either rotation or the caloric test. 

The clinical features of these cases usually leave in doubt the question as 
to whether the membranous labyrinth or the eighth nerve is the structure 
primarily attacked. Involvement of other cranial nerves and simultaneous 
and equal disturbance of both cochlear and vestibular functions would point 
to the nerve as the structure primarily attacked; while the escape of other 
cranial nerves plus unequal disturbance of the two branches of the eighth 
nerve would point rather strongly to a direct invasion of the labyrinth. 

Aside from the very characteristic onset of the attack in a person whose 
drum membranes may show no morbid changes, there are usually other 
evidences of the disease in cuticular eruptions, mucous patches, etc., 
which, in conjunction with the history of an initial lesion, may leave no 
doubt as to the syphilitic origin of the labyrinthine disorder. 

Though necessarily causing great anxiety, the prognosis is more fa¬ 
vorable than in any other form of syphilitic labyrinthitis. The treatment, 
which is practically the same as for syphilitic affections of the cranial 
nerves, will be discussed somewhat fully in the chapter devoted to the 
use of salvarsan in aural disease (see Chapter xxi). 

(3) Another clinical variety of the disease, the pathologic basis of 
which is not always so easily determined, is found in adults who have 
suffered from chronic constitutional syphilis over a period of years. The 
drum membranes may or may not show evidences of tympanic disease, 
which, if present, may represent an intercurrent and pathologically inde¬ 
pendent lesion. Such a patient frequently gives a history of occasional 
attacks of vertigo of more or less pronounced type, or such attacks, having 
belonged to an earlier stage of the disease, may have ceased to annoy 
him. The diagnosis depends chiefly upon the labyrinthine character of 
the deafness,— i.e., diminished bone conduction, negative Rinne, loss of 
hearing for the highest musical tone,—plus constitutional evidences of 
the disease. Very frequently the pharynx and nasal cavities show the 
cicatrices and perforations representing the typical lesions of an earlier stage. 

Naturally the history of such a patient might be expected to furnish data 
of considerable diagnostic significance. To other manifestations of the dis¬ 
ease the Wassermann test contributes the strongest corroborative evidence. 

The lesion from which it is in some cases most difficult to differentiate 


3 Kerrison: Vertigo of Vestibular Paralysis, Transactions Amer. Otol. Soc., 1911. 









532 


NON-SUPPURATIVE DISEASES OF LABYRINTH 


chronic syphilitic labyrinthitis is that form of otosclerosis which involves not 
only the labyrinthine capsule but also the membranous cochlea. Between 
these two conditions a positive differentiation is not in all cases possible. 
The history of a very sudden development of the deafness, coming on in 
the late secondary or in the tertiary stage of acquired syphilis, would go far 
toward establishing the syphilitic character of the labyrinthine lesion. 

The treatment in these cases is the treatment of chronic syphilis. The 
prognosis, so far as any marked improvement of hearing is concerned, 
is unfavorable. 

(4) The fourth clinical type may be dealt with briefly. It is found in 
patients who are victims of constitutional syphilis of long standing, and 
whose ears exhibit the physical characteristics of a middle-ear suppura¬ 
tion (usually of offensive type) and the functional reactions of labyrinthine 
disease. The syphilitic nature of the labyrinthine lesion is usually an hy¬ 
pothesis not susceptible of definite proof. It is, however, an hypothesis of 
very practical importance, for the reason that improvement, either func¬ 
tional or of the concomitant suppurative lesion of the middle ear, is not 
likely to result from any plan of local treatment not reinforced by active 
measures to eradicate the constitutional disease. 

Treatment. —There is no manifestation of syphilis which calls more 
urgently for vigorous efforts to eradicate the systemic poison than syphi¬ 
litic labyrinthitis. The question of treatment resolves itself into a com¬ 
parison of the few drugs of known value, and the best methods of admin¬ 
istering them. The more important phases of this subject are discussed 
in the chapter devoted to the use of salvarsan in aural therapy. 

Tuberculosis of the Ear. —Tuberculous lesions of the ear usually attack 
first the tympanum, and such lesions, more than any other form of middle- 
ear disease, are prone to cause extensive caries or necrosis of the labyrin¬ 
thine capsule. It would be quite illogical, therefore, to speak of tuber¬ 
culosis of the tympanum and of the labyrinth as distinct pathological 
entities, or to consider them under separate headings. 

The tubercle bacilli may reach the ear by the blood or lymph channels, 
but unquestionably the commoner pathway is by the Eustachian canal. 

The predisposing causes are (1) inherited predisposition to tuber¬ 
culosis; (2) environment, i.e., unfavorable surroundings and conditions 
of life; and (3) age, children being more subject than adults to the disease. 

The influence of heredity is shown in the case of individuals inheriting the 
so-called tubercular diathesis, who undoubtedly are more likely to develop 
primary tuberculous lesions of the middle ear, and in whom the common 
type of suppurative otitis media is more likely to be converted into a tuber¬ 
culous lesion than is the case with an individual of normal resistance. 

The influence of environment is seen in the comparative frequency of 
tuberculous middle-ear lesions among the poorer class of tenement-house 
dwellers, who have to contend not only with overcrowding and poor 
ventilation, but often also with the effects of poor and insufficient food. 
The influence of such conditions is twofold,— i.e., (a) by reducing the 


TUBERCULOSIS OF THE EAR 


533 


individual’s power of resistance to any form of disease, and (b) by his 
unavoidable proximity to, and association with, tuberculous individuals 
not suspected of harboring the disease. 

Age is a predisposing factor to the extent that infants and young chil¬ 
dren are particularly subject to tuberculous affections of the middle ear. 
The greater predisposition of the child as compared with the adult is 
illustrated again in the children of the tenements, and particularly when 
they are attacked by one or other of the acute infectious diseases,— e.g., 
scarlet fever, measles, etc. The very rapid and extensive destruction of 
the drum membrane and of the bony structures of the tympanum so fre¬ 
quently seen in children suffering from scarlet fever is undoubtedly ex¬ 
plained in many cases by a tuberculous element in the pathology of the 
tympanic lesion. To some extent the greater vulnerability of the very 
young child to tuberculous middle-ear disease is due to certain anatomical 
peculiarities of the infantile type of Eustachian tube (see page 154), in 
consequence of which the middle ear of the child is more open than in the 
adult to the entrance of infective material from the nasopharynx. 

If we will picture to ourselves a condition by no means uncommon in 
crowded cities,— i.e., of a child, ill-nourished and reduced by unhealthy 
surroundings; breathing an atmosphere in which tubercle bacilli are prob¬ 
ably often present; the presence of adenoids in which many germs, and 
perhaps tubercle bacilli, find lodgment; add to this a possible inheritance 
of predisposition to tuberculous infection, and an igniting spark in the 
form of an acute infectious disease, and we have an ideal condition for the 
development of a primary tuberculous lesion of the tympanum. 

Among adults tuberculosis of the middle ear occurs most frequently 
in patients in advanced stages of phthisis. It occurs, however, even during 
the earliest stages of pulmonary tuberculosis, and authenticated cases have 
been recorded in which no other tuberculous lesion could be determined. 

Pathology. —A tuberculous attack upon a previously healthy ear is 
marked by the following changes: The tympanic mucosa is swollen or 
oedematous, this condition involving the lining membrane of the promon¬ 
tory and contiguous bony surfaces and to some extent the inner lining of 
the drum membrane. Small circumscribed thickenings, seen here and 
there, represent the tubercle nodules. Similar nodules are formed upon 
the drum membrane, and partly explain one of the characteristic clinical 
features of the disease which will be referred to later. Under the micro¬ 
scope, sections of the diseased mucosa show widespread infiltration with 
small cells, with here and there groups of giant cells, and a varying number 
of tubercle bacilli. This represents a fairly early stage, which is followed, 
usually rather quickly, by breaking down of the nodules and the formation of 
granulations which under the microscope are seen to contain giant cells and 
usually tubercle bacilli. Breaking down of the nodules upon the drum mem¬ 
brane is followed by circumscribed points of ulceration which may involve 
the entire thickness of the membrana tensa, thus giving rise to the multiple 
perforations which form so characteristic a feature of the disease. 


534 


NON-SUPPURATIVE DISEASES OF LABYRINTH 


Following the breaking down of the nodules upon the bony wall of 
the tympanum, the mucous membrane undergoes rather rapid and wide¬ 
spread destruction, and caries of the underlying bone is a frequent and 
somewhat characteristic phenomenon. It is also highly characteristic of 
middle-ear tuberculosis that osseous necrosis spreads rapidly and widely, 
while the usual clinical phenomena of pain, bone tenderness, and fever 
are either absent or infinitely less pronounced than usually attend the 
rapid extension through bone of a suppurative process of streptococcic 
origin. Another distinctly characteristic feature of tuberculous tympano- 
mastoiditis is the tendency to the formation of large sequestra, which, 
if operative intervention is withheld, detach themselves and occasionally 
are extruded through the auditory meatus or through a postauricular 
sinus. Still another pathologic feature, which is characteristic of this 
lesion, is the frequency with which the disease involves large portions of 
the labyrinthine capsule without producing any of the usual phenomena 
of vestibular irritation. The'Fallopian canal is logically a vulnerable 
structure in the presence of such a lesion, and facial paralysis, dependent 
upon tuberculous changes actually involving the nerve itself, is a common 
feature of advanced middle-ear tuberculosis. While the formation of 
granulations within the tympanum is characteristic of an early stage of 
the lesion, they may disappear later, leaving bare tympanic walls pre¬ 
senting a bloodless appearance. 

The above account describes in brief the characteristic changes in a 
case of aural tuberculosis in which infection has occurred by way of the - 
Eustachian canal. There is, however, another mode of invasion, in which 
the mastoid is apparently the primary point of attack, the tympanic 
structures being involved later. Bryant explains such cases as being due 
to a tuberculous infection of the lymphatic glands in the region of the 
mastoid. Described in stages, the pathologic changes following this mode 
of infection are said to occur in the following sequence: (a) Enlargement 
of lymphatic glands over mastoid; (b) postauricular periostitis and oedema; 
(c) cortical bone involvement with moderate bone tenderness, and (d) 
rapid extension of the lesion through the intercellular structures of the 
mastoid to the middle ear. 

Symptoms. —The patient, usually without prodromal symptoms, may 
experience moderate pain or only a sense of discomfort in the ear, or the 
early changes may occur without any symptoms sufficiently pronounced 
to attract his attention. In the latter case his first intimation of aural 
disease may be a slight discharge from the ear. The discharge at first is 
usually watery, turbid, or slightly bloody. If the ear is examined before 
rupture has taken place, it will usually present an cedematous appear¬ 
ance, sometimes showing moderate congestion, but rarely the angry red 
color characteristic of the ordinary forms of tympanic inflammation. 
Here and there over the membrana tensa are seen small millet-seed pro¬ 
jections, pearl-gray in color, representing tuberculous nodules. At a later 
stage one or more of these nodular points will be seen to have given place 


TUBERCULOSIS OF THE EAR 


535 


to circumscribed perforations, which still later are apt to become con¬ 
fluent, resulting ultimately in widespread or almost complete destruction 
of the drum-head. When the lesion is well advanced, bare bone may 
usually either be seen upon the inner tympanic wall or detected beneath 
flabby granulations by means of the probe. During all of the above 
changes the patient may experience practically no aural pain. As the 
disease advances, involvement of the labyrinthine capsule may be shown 
by impairment of hearing, and of course in some cases by disturbances of 
equilibrium. Facial paralysis is said to occur in about 50 per cent, of cases. 
The lymphatic glands in the region of the mastoid and in front of the 
tragus are enlarged in a majority of cases. Later the glands in front 
of the sternomastoid muscle are also involved. In the later stages of the 
disease, the aural discharge is usually more profuse and also more offensive. 
The characteristic disintegration of tissue may extend to the ossicular 
ligaments, as a result of which the ossicles may fall out. Crockett has 
reported cases in which the malleus or incus has come away with the 
solution used in irrigating the ear; and Seymour Oppenheimer has recorded 
a case in which the patient, attempting to wipe out the ear with a cotton- 
wound applicator, found adhering to the cotton the entire ossicular chain. 4 

Diagnosis. —To epitomize: The diagnosis depends on the compara¬ 
tively painless onset; the early oedematous, rather than acutely inflamed, 
appearance of the drum membrane; the appearance upon the drum-head 
of minute, grayish nodules, giving place later to multiple perforations; 
the rapid destruction of drum membrane and of the tympanic mucosa; 
the frequent presence of facial paresis or paralysis; the presence of gland¬ 
ular swelling over the mastoid, and particularly of a small glandular 
swelling in front of the tragus (Crockett). During operations upon the 
mastoid, the evidences of very extensive osseous necrosis, with the presence 
of large and partially detached sequestra, are highly characteristic either 
of a lesion tuberculous from its incipiency, or of a mixed infection in 
which a tuberculous element is the dominating factor. 

Naturally a decisive diagnostic point in all cases of tuberculosis of the 
middle ear would be the presence of tubercle bacilli in the aural discharge. 
It is often difficult or impossible, however, to demonstrate the bacilli in 
the thin, watery secretion of the early stages of the disease, so that absence 
of demonstrable bacilli can not be taken as disproof of the disease. 

Terminations. —It is difficult to speak authoritatively of the termi¬ 
nations of tuberculous disease of the tympanum, for the reason that tuber¬ 
culosis primary in and confined to the middle ear and mastoid usually 
responds favorably to early treatment, whereas a tympanic lesion second¬ 
ary to pulmonary tuberculosis usually succumbs to the pulmonary lesion. 
It is an interesting and somewhat unaccountable fact that tympanic 
tuberculosis rarely leads to tuberculous meningitis, though such extension 

is known to occu r (McCaw). _____ 

' 4 Oppenheimer, S. : Pathology, Diagnosis, and Treatment of Tuberculosis of the 
Middle Ear, Medical Record, Nov. 24, 1900. 







536 


NON-SUPPURATIVE DISEASES OF LABYRINTH 


A question which in the past has been the subject of considerable 
controversy is whether tuberculosis of the middle ear can occur as a 
primary lesion or is always secondary to a lesion in the lungs or elsewhere 
in the body. Apparently there is no longer reason to doubt that primary 
tympanic lesions do occur, and that under skilful treatment they offer a 
fairly good prognosis. In Europe the work of Habermann and of Milligan 
has thrown considerable light on this question. In America, cases of 
tuberculosis confined to the ear have been reported by Goldstein, Crockett, 
McCaw, and others, and a fair proportion of these cases have recovered 
wholly, and apparently permanently, under prompt and wise surgical 
treatment. While children furnish a majority of the cases of primary 
middle-ear tuberculosis, adults are by no means immune. Two of Gold¬ 
stein’s four cases occurred in adults. 5 McCaw’s 6 case was that of a man 
who, without at any time presenting symptoms of pulmonary tubercu¬ 
losis, contracted a tuberculous lesion of the left middle ear. Clinically 
the disease presented all the classical features of tympanic tuberculosis, 
ending, however, in tuberculous meningitis, a somewhat rare termination. 
Operation showed widespread osseous necrosis and the dura in the region 
of the destroyed tegmen antri greatly thickened and studded with miliary 
tubercles. Autopsy showed lungs, liver, spleen, and kidneys free from 
any signs of tuberculous change and the mesenteric glands not enlarged. 
This apparently was a primary tuberculous lesion of the ear, to which 
the disease was confined up to the fatal implication of the meninges. 
Bryant 7 has recorded an exceedingly interesting case in which a tuber¬ 
culous lesion of the middle ear was positively diagnosticated in a man, 
apparently in robust health, who, though frequently examined, presented 
no symptoms of pulmonary tuberculosis until six months later. Bryant’s 
interpretation of this case is that the pulmonary lesion was the primary 
focus, from which hypothesis he makes the deduction that one may be able 
to diagnosticate pulmonary tuberculosis from tuberculous changes in the ear 
long before pulmonary symptoms are present. There is nothing in Bryant’s 
history of the case, however, to prove this sequence, and there seems no reason 
why the hypothesis may not be reversed,— i.e., that the aural disease was 
the primary focus to which the pulmonary lesion was secondary. 

Prognosis. — In a majority of adult cases, the tympanic lesion is 
secondary to an advanced stage of pulmonary phthisis, in which case the 
prognosis is wholly unfavorable. When a primary tympanic lesion is 
diagnosticated early and brought under rational treatment, the chances 
of recovery are fairly good. Crockett, 8 who has reported a small but 


6 Goldstein, M. A.: Primary Tuberculosis of the Ear, etc., Medical News, March 
14, 1903. 

6 McCaw, J. F.: Tuberculous Otitis Media in an Otherwise Healthy Adult, Medical 
News, Oct. 12, 1901. 

7 Bryant, W. S.: Tuberculosis of the Ear, Medical Record, Sept. 26, 1908. 

8 Crockett, E. H.: Tuberculosis of the Middle Ear and Mastoid, Jour. Amer. Med. 
Assoc., Oct. 20, 1906. 



TUBERCULOSIS OF THE EAR 


537 


exceedingly interesting series of cases in children, records his belief that 
primary tuberculosis of the middle ear and mastoid should be treated by 
prompt surgical removal of all diseased bone, under which plan of treat¬ 
ment he regards the prognosis as quite as favorable as in the severe mas¬ 
toid lesions of suppurative type complicating scarlet fever. 

Treatment. —Aside from local cleanliness, it is perhaps best not to 
place undue emphasis upon the local treatment of these cases. It is a 
recognized fact that syringing the ears is injurious in tuberculous otitis 
media. The cleansing must, therefore, for the most part be accomplished 
by wiping the ear out with sterile cotton. Powders— e.g., of boric acid, 
xeroform, etc.—help to keep the ear clean and dry. The throat and nose 
should be kept as free as possible from pathogenic bacteria by the use of 
antiseptic sprays and gargles. 

Quite as important as the local treatment is the management of the 
patient's life. Change of climate, the arrangement of the sleeping apart¬ 
ment, freedom from care and nerve-strain, life in the open air, the use of 
constructive tonics and the most nutritious and easily digested diet play 
as important a role as in pulmonary tuberculosis; for they not only influ¬ 
ence the outcome of the aural lesion, but also go far to prevent secondary 
invasion of the lungs, a consideration which should never be lost sight of 
in dealing with primary tuberculous lesions of the ear. 

As to the question of operating, that should be decided only after a 
consideration of all the facts bearing upon each particular case. In the 
first place, it is well to bear in mind that many cases of middle-ear tuber¬ 
culosis have recovered wholly under rational constitutional and hygienic 
management, with no other local treatment than measures for cleansing 
the ears. Crockett has recorded several instances of apparently complete 
recovery under such conservative methods of treatment. On the other 
hand, in the presence of a rapidly-spreading bone lesion primary in and 
confined to the ear, there would seem to be no question that thorough 
eradication of all diseased bone by a careful Schwartze-Stacke operation 
provides the only logical course and offers the best promise of recovery. 

Undoubtedly the most difficult problems may be presented in cases in 
which tympanic and pulmonary lesions coexist. With pulmonary phthisis 
well advanced, it is clear that a mastoid operation, even though otherwise 
clearly indicated, may involve great risks in the influence it might exert 
upon the progress of the lesion in the lung. The correct course to pursue 
in such cases does not provide a favorable theme for dogmatic statement. 
If the pulmonary lesion has reached a stage at which recovery may not 
be hoped for, a mastoid operation would be quite unjustifiable. On the 
other hand, cases undoubtedly occur in which a timely opening of the 
mastoid would constitute an essential step in the treatment of pulmonary 

tuberculosis. 


CHAPTER XXII. 


OTOLOGIC LESSONS OF THE WORLD WAR. 

WAR DEAFNESS: DEAFNESS DUE TO DIRECT LABYRINTHINE INJURY: 

CONCUSSION DEAFNESS: PSYCHIC DEAFNESS: PITHIATISM 
SIMULATION: PITHIATIC DEAFNESS: DIAGNOSIS AND 
RATIONALE OF TREATMENT. 

Probably most of us have heard the remark that the war has added little 
to our knowledge applicable to the peace-time practice of medicine. This, 
for the moment, may be true, since the men whose opportunities for ob¬ 
servation and deduction have been greatest have hardly yet had time to 
correlate and systematize their experiences. Even less has the profession 
at large had time to digest and assimilate the published facts. 

As to the surgical experiences of the war, only those who have actually 
observed or practiced it are in a position at the present time to speak. Yet, 
whoever reads even such fragmentary accounts as have so far reached us 
will surely come upon statements of actual experience, reflections on phe¬ 
nomena observed, interpretations of unfamiliar syndromes, modifications of 
classical surgical procedure, etc., etc., which cannot fail to stimulate thought 
and awaken a desire to review our time-honored theories and methods in the 
light of the accumulated data of the war. To illustrate my meaning:—let 
us take for example a comparatively simple accident, i.e., the linear or 
stellate rupture of the drumhead occasionally resulting from a forcible slap, 
or “box on the ear. ” We are accustomed to regard the rupture of the mem¬ 
brane, on account of its possible sequelae, as the most serious result of this 
outrage. But in his study of cases of deafness produced by the concussion 
of loud and near-by explosions, Bourgeois has observed that in those, cases 
in which the drum membrane is ruptured, the injury of the perceptive 
labyrinth and the consequent deafness are less grave and less apt to be per¬ 
manent than in cases in which the drum membrane remains intact. The 
logic of this observation is clear: for if the first- force of the air condensation 
is expended in rupturing the drumhead, it is obvious that this structure 
cannot carry the hammer handle and with it the incus and foot-plate of the 
stapes suddenly and forcibly inward, and the insult to the membranous 
labyrinth is lessened. A further conservative influence is the fact that, 
with the rupture of the drumhead, air entering the tympanum, acts simul¬ 
taneously on the stapes and membrane of the round window, thereby de¬ 
stroying their compensatory function and thus lessening or inhibiting the 
movements of the labyrinthine fluids. We must, therefore, hereafter regard 
the accident to the drumhead following a blow on the ear as an unfortunate 
accident but, nevertheless, as the lesser of two possible evils. Again, 

Bourgeois formulates a rule as fully established by the experiences of the 
538 


WAR DEAFNESS 


539 


war that accidents to the ear resulting in rupture of the drum membrane 
should not he irrigated nor treated with bactericidal drops. Instead, the ear and 
canal should be cleansed as far as possible with drysteiile cotton and then 
protected from germs from without. May we not draw from this some uselul 
deductions as to our routine methods in the treatment of certain lesions? 

In the line of major operations, we may mention that of Professor Moure 
for accidents of the mastoid or tympanic region resulting in facial paralysis. 
Having widely exposed the tympanic and mastoid fields, Moure makes a 
careful and systematic exposure of the facial nerve, beginning his uncover¬ 
ing of the Fallopian canal just over the fenestra ovalis and thence tracing 
the nerve backward and downward to its exit from the canal at the stylo¬ 
mastoid foramen. If the nerve is found intact, even though bruised, he is 
content with having removed pressure; if divided, the ends are sutured. If 
this very logical operation is possible in war time surgery, surely it should be 
more so in times of peace. And if successful, how obvious the advantages 
over the older operations for engrafting the peripheral segment of the in¬ 
jured facial into the sound trunk of another cranial nerve. 

But valuable as the lessons in aural surgery may ultimately prove to be, 
there is another chapter of the medical history of the war in which otologists 
are more deeply interested, i.e., that which deals with the various types of 
war deafness. These functional disturbances vary with the agency produc¬ 
ing the injury, the character and site of the lesion, the position ol the person 
at the time of the injury (i.e., whether in the open or in a confined space, e.g., 
trench) and finally with the morale, or mental and nervous organization, ot 
the individual. Evidently there are certain injuries which by their de¬ 
structive character must produce absolute or profound and permanent 
deafness. There are other injuries followed by a deafness equally profound, 
which eventuate in more or less rapid amelioration or recovery. And since 
in certain cases the deafness produced by these lesser injuries fails to ex¬ 
hibit the expected amelioration, even though the labyrinth may show in eei- 
tain directions normal reactions, the conclusion is reached that under cer¬ 
tain conditions a deafness originally induced by an insult to the perceptive 
labyrinth may be maintained or perpetuated through a psychic disorder. 
In other words, there is a type of war deafness which can be correctly inter¬ 
preted only as a psychosis. 

For various and obvious reasons what has been learned of the deafness 
resulting from near-by explosions as well as that resulting from direct 
cranial injuries by projectiles, bits of shrapnel, etc., has been based upon 
the clinical phenomena observed, and to a very limited extent only upon 

post-mortem studies. . 

According to Bourgeois, no organic lesions of the labyrinth have been 

observed or recorded as a result of injuries primarily involving only the 
soft parts, even in the case of so intimate a structure as the membranous 

auditory canal. ., . „ . . 

Of direct cranial injuries, those of the mastoid region natuialR m\o \e 

the labyrinth in the largest percentage of cases. According to the 


540 


OTOLOGIC LESSONS OF THE WORLD WAR 


statistics of Lannois and Chavanne, 1 in 38 cases of direct wounds of the 
mastoid region, total deafness resulted in 73 per cent, and partial deafness 
in 21 per cent, of cases. In the 23 cases constituting the statistics of Bour¬ 
geois, 60 per cent, and 33 per cent, resulted in total and partial deafness 
respectively. Next to the mastoid comes the temporo-maxillary region in 
the frequency of actual injury to the labyrinth, with deafness in 66 per 
cent, of cases. In half of these cases the deafness was absolute; in the 
reminder, partial. Of other parts of the skull, injuries of the occipital 
and temporo-parietal regions frequently involve the labyrinth (Chatelin). 
On the other hand, serious injury to the labyrinth as a result of military 
wounds of the frontal region is comparatively rare. 

According to Bourgeois, the disturbances of hearing are more con¬ 
spicuous than the disturbances of equilibrium in lesions of the labyrinth 
resulting from direct cranial injuries. This does not mean that the static 
labyrinths do not suffer, but that by comparison with the deafness, the 
disturbances of equilibrium often seem inconspicuous. Bourgeois states his 
belief that the deafness caused by a fracture involving the labyrinth is total 
and permanent. Naturally, these cases as a rule exhibit disturbances of equi¬ 
librium in the days immediately following the injury, but even in cases caus¬ 
ing permanent and absolute deafness, he believes that the vertigo, subjective 
and objective, disappears wholly in time. This, of course, is in accordance 
with what we know of the sequence of events in other lesions of the labyrinth. 

Fortunately, in the great majority of cranial wounds resulting in serious 
lesions of the labyrinth, only one labyrinth is involved, i.e., that correspond¬ 
ing to the side of the cranial injury. 

Of the actual pathology of these wounds, but little need be said since 
there has been little or no opportunity to check up clinical observations by 
properly conducted post-mortem examinations. When cranial injuries have 
been followed by profound and apparently permanent deafness, destructive 
changes in the labyrinth have been assumed, whereas a partial deafness or 
an immediately profound or absolute deafness showing more or less rapid 
or progressive amelioration naturally leads to a different conception of the 
nature of the labyrinthine lesion. 

As to the pathogenesis of organic lesions of the labyrinth resulting from 
direct cranial wounds, different views are held by different observers. Le 
Mee and Toubert 2 believe that all organic labyrinthine lesions complicating 
cranial wounds are the result of gross or minute fractures of the labyrinthine 
capsule, produced either by direct violence upon the labyrinth or by ex¬ 
tension from fractures of the base of the skull or from fractures extending 
downward from the temporo-parietal region. With this view Lannois, 
Chavanne and Bourgeois do not agree: recognizing fractures, gross or 
microscopic, of the labyrinthine capsule as occasional and possibly fre¬ 
quent war time lesions, these writers hold that rupture of minute blood 
vessels or tearing of terminal nerve filaments either of which might cause 
destructive or degenerative changes within the labyrinth, may be caused by 


1 Quoted by Bourgeois and Sourdille. 

2 Quoted by Bourgeois and Sourdille. 





CONCUSSION DEAFNESS 


541 


cranial injuries which produce absolutely no loss of continuity of the laby¬ 
rinthine capsule. Considering the extreme delicacy of certain parts of the 
membranous labyrinth and the intense commotion and pressure to which 
they may be exposed by the severer cranial injuries, the latter view seems 
based on better logic. 

From the foregoing statements, particularly as to the high percentages 
of absolute and permanent deafness, one's first impression is of a vast aggre¬ 
gate destruction of hearing in the late war. Deplorably great it probably 
has been. But we must remember that the percentages so far given have 
referred only to the cases of deafness due to direct cranial injury; and that 
such cases, when compared with those of deafness due to other and lesser 
causes, form so small a minority as almost to justify their being spoken of 
as among the rarer mishaps of the war. 

Concussion Deafness Due to Explosions .—All observers are apparently 
agreed that great numbers of men suffered deafness of varying degrees and of 
various periods of duration as a result of air concussion, or the sudden and 
great displacement and condensation of air incident to near-by explosions. 
As regards this class of cases, certain facts apparently stand out. (1) While 
it is conceded that an aerial concussion from a near-by explosion or even 
under certain conditions from the firing of large cannon, may produce such 
violent disturbance of the cochlear structures as permanently to destroy 
their function, the consensus of opinion is that such cases are comparatively 
rare. Complete and permanent deafness is therefore exceptional. (2) 
Deafness due to concussion is usually unilateral, and confined to the ear 
nearest the explosive sound, i.e., provided that at the time of the explosion 
the individual is in the open. It may be, and usually is, bilateral, when 
caused by an explosion while he is in a confined space, e.g., dug-out or 
trench. (3) In cases of labyrinthine disturbance due to concussion from loud 
explosive noises, the cochlear mechanism is regularly more affected than the 
vestibular apparatus. As a rule the vestibular mechanism escapes wholly. 

As throwing a considerable and very practical light on concussion 
deafness, the experiments of Prenant and Castex 3 are exceedingly interesting 
and instructive. These investigators subjected rabbits and guinea pigs to 
the detonations of heavy cannon of modern type, and then made careful 
observations of the labyrinthine changes induced. The following changes 
were noted: (a) dislocations of the ductus cochlearis, frequently with 
destructive changes in Corti’s organ, (b) Effusion of blood in scala tympani 
due to rupture of minute vessels, (c) Atrophy of Organ of Corti and of all 
structures on cochlear surface of basilar membrane, (d) Apparent atrophy 
of ganglionic cells of the spiral ganglion, (e) (Rare) degenerative changes 
in central fibres of cochlear nerve. Perhaps the most important observa¬ 
tion in the diagnostic light it throws on these cases is the negative finding, 
(f) “Integrity of the organs of the static sense noted in every case. 

V The pathologic findings in the experiments above quoted are extremely 


3 Prenant and Castex, quoted by Bourgeois: War Otitis and Deafness, Pp. 89, 90. 






542 


OTOLOGIC LESSONS OF THE WORLD WAR 


important in that they supply the most clear-cut differential point between 
the labyrinthine lesions due to direct cranial injuries and those of the 
severest type (■ i.e., causing absolute and permanent deafness) due to aerial 
concussion. If we admit that cranial injuries involving the labyrinth are 
likely to, or in fact almost of necessity must, involve both the cochlear and 
vestibular portions, and that the severest aerial concussions involve only 
the cochlear apparatus, it is clear that the ultimate clinical aspects of the 
severest t}^pes of these two lesions will be: (a) in the case of the labyrinthine 
lesion secondary to direct cranial injury, absolute deafness plus a non-irri- 
table vestibular mechanism ( e.g ., to cold or heat); and (b) in the case of a 
severe labyrinthine lesion from concussion, deafness advanced or absolute , 
with retention of a normally functionating static labyrinth. 

The comparative immunity of the vestibular and semicircular canal 
system from serious injury by concussion, even following the loudest de¬ 
tonations, will become clear to us if we consider certain differences in the 
physiology of the two mechanisms of the labyrinth. The cochlear mechan¬ 
ism, specialized for reacting only to sound waves from without, is naturally 
subjected to a disturbance by any convulsion in the surrounding air in direct 
proportion to its violence. The fluids and structures of the vestibular mechan¬ 
ism, on the other hand, being normally uninfluenced by any agency from with¬ 
out, and reacting only to changes in the position of the head, are practically 
shielded from disturbances of the air induced by explosions. It is probable 
that the disturbances of equilibrium following explosions are induced either 
as a sympathetic phenomenon on account of its close association with the 
anterior (cochlear) labyrinth, or perhaps in certain cases from the individ¬ 
ual’s being thrown with more or less violence by the force of the explosion. 

All grades of concussion deafness are said to have followed every heavy 
artillery engagement or action. They have varied from comparatively slight 
impairment to profound or absolute deafness. Naturally in a continued en¬ 
gagement both ears are subject to the same disturbance,—so that the milder 
cases are frequently bilateral. As a rule fairly rapid functional improvement 
has occurred in the milder cases, and even in cases of immediately profound 
or absolute deafness, beginning recovery of function has in many cases been 
an early phenomenon. Naturally in the severest injuries recoveries have been 
slower and ultimately only partial. But the cases of complete and permanent 
deafness from concussion appear to have been comparatively rare. 

As to the character of the deafness, this, from all reports, is the same in 
kind whatever the character of the injury which has caused it,— e.g., 
diminution or loss of hearing alike by air and bone conduction. When the 
deafness is not absolute, therefore, Rinne may remain positive, though it is 
clear that an apparently negative Rinne may be present through the con¬ 
duction of sound waves through the cranial bones to the sound ear. Weber 
is referred to the sound ear. The upper limit of tone perception is markedly 
reduced. These changes characterize the deafness due either to concussion 
or to direct labyrinthine injury up to the point of total deafness, when all 
differential points, other than the degree of deafness itself, fail. 


HYSTERICAL OR PSYCHIC DEAFNESS 


543 


In cases of very extreme or absolute deafness, the chief reliance in 
the differential diagnosis between cases due to a direct injury of the laby¬ 
rinth (e.g., through fracture of the capsule) and those due to a cochlear de¬ 
generation from concussion (e.g., following the explosion of a mine or large 
projectile) is apparently the loss or persistence of the normal vestibular re¬ 
flexes, e.g., reactions to heat or cold. The importance of a correct differen¬ 
tiation is not merely academic, since the prognosis even in extreme cases of 
concussion deafness is known to be infinitely more hopeful than in cases of 
deafness from wounds directly involving the skull. 

Hysterical or Psychic Deafness: Pithiatism: Psychic Mutism: Simu¬ 
lation. —Hysterical deafness has been a convenient term in otology, a substi¬ 
tute for a confession of ignorance,—a term, that is to say, which calls up or 
conveys no mental picture of any definite aural disorder. Babinski and 
Froment have utilized the rich clinical material of the war as a means to re¬ 
test the theory of auditory hysteria, and have more clearly defined its 
meaning, its limitations and its varying clinical aspects. Independent 
observations and investigations by Secard and Beilin, by Brindel, by Gault 
and by Bourgeois of various phases of so-called functional deafness have on 
the whole brought support to their conclusions. For hysteria Babinski has 
substituted a new and more descriptive word, pithiatism, a term deiived 
from two Greek words and meaning curable by persuasion. 

Pithiatism implies not only the possibility of cure by persuasion, but also 
the fact that the disorder may in some degree be called into being by sug¬ 
gestion. This does not mean that the origin of a pithiatic disorder is of 
necessity a hallucination or purely imaginary. Pithiatic deal ness, foi ex¬ 
ample, as we shall see, is at its inception a veritable deafness, the inevitable 
sequence of a shock to the perceptive labyrinth which could have had no 
other result. So far it has no hysterical or pithiatic character. But as the 
actual functional disability begins to subside, other factors, psychic in char¬ 
acter, come into play and finally gain ascendence. To the extent to which 
thev interfere with a normal recovery, the disorder then takes on a hysteri¬ 
cal, or pithiatic, character. 

There can be no question that the late war has created an ideal environ¬ 
ment for the class of disorders under discussion. We are to picture to our¬ 
selves vast numbers of men of all social strata, of all degrees of intellectual 
poverty or attainment, of all grades of moral stamina or weakness, diagged 
suddenly from home and family ties, subjected for weeks or months to dis¬ 
piriting monotony, to physical and mental tortures of heat or cold, of nerve- 
racking fatigue, of heart-piercing anxieties for unprotected dependents at 
home, of brooding doubts and fears as to unknown but impending ordeals. 
We must picture these men hurled suddenly into an inferno of carnage, a 
chaos of sights and sounds of such frightfulness and terror as men have never 
faced before,—and we have a fitting laboratory in which to observe and 

study the origin and incipient phases ol pithiatism. . 

After the engagement our patient, with or without other physical in¬ 
juries, suddenly realizes that he is profoundly deaf. He has seen men killed 


544 


OTOLOGIC LESSONS OF THE WORLD WAR 


or mangled before his eyes; he has heard of others made totally and per¬ 
manently blind. The sudden loss of hearing, superadded to the depression 
of deadly physical fatigue, typifies in his mind the scope and gravity of the 
catastrophe which has overtaken him. Though he may accept his condi¬ 
tion without complaint, he feels that his usefulness is permanently impaired. 
Since he is obviously incapacitated for receiving and carrying out orders, 
he is sent to a hospital for observation and treatment. 

At the hospital or observation camp his hearing is tested and the pro¬ 
nounced character of his auditory defect verified; and a course of treatment 
planned. But whether the physician in charge has or has not been able to 
correctly interpret his condition, its treatment in reality must meet two 
quite distinct problems: (a) to bring about a restoration of the auditory 
function (and for this the element of time is probably the chief factor) and 
(b) to convince the patient of the progress of his recovery. As the days or 
weeks pass, the patient’s general physical and nervous condition responds 
to rest and care, but deaf, and hopelessly deaf, he still believes himself to be. 

One factor which is said in certain hospitals or observation camps to 
have fostered this hallucination in a patient in spite of returning function, 
has been the fact of other actually permanently deaf individuals associated 
with him in a common routine plan of treatment, their failure to show any 
favorable response impressing him with a hopeless prognostic view of his 
own condition. Such a patient may become a typical pithiatic. He honestly 
regards himself as hopelessly deaf and loses interest in his own recovery; nor 
is he likely to exhibit a more healthy mental state unless he comes under the 
care of a physician who understands his condition and how to deal with it. 

While all classes of men are subject to pithiatic deafness, it is said that 
men of low mental status and of little education are particularly prone to 
become its victims. 

Several phases of pithiatic deafness conspire to obscure the diagnosis for 
a physician unfamiliar with the condition. In the first place, even after 
actual auditory recovery is in progress, the healing is still impaired. To 
hear and understand conversational speech, therefore, requires effort; and 
this effort the pithiatic, harboring the obsession of permanent deafness, 
will not make. Such is his lethargy that his responses to hearing tests do 
not fairly represent his actual auditory ability. 

As to how far wilful, or intentional, simulation or malingering may play 
a part in any given case may be a difficult point to determine. It is at least 
apparent, however, that a man who has philosophised over his deafness as 
permanent and therefore to be accepted, may appreciate certain compensa¬ 
tory advantages,— e.g., immunity from active military service, etc. How 
these two psychic factors may react upon each other, and which may pre¬ 
ponderate, may call for keen analysis as well as a broad and tolerantly 
human viewpoint. 

Bourgeois describes three types of pithiatic deafness: (a) deafmutism; 
(b) absolute deafness, and (c) partial, though pronounced, deafness. Deaf¬ 
mutism excites suspicion (1) from the fact that acquired total and perma- 


GAULT’S COCHLEO-PALPEBRAL TEST 


545 


nent bilateral deafness is exceedingly rare; and (2) even absolute deafness of 
recent development does not usually produce mutism. Absolute deafness and 
extreme hardness of hearing are not usually difficult to gauge, but an added 
element of either pithiatism or intentional simulation increases the difficulty. 

One thing must be clear from what has been said, i.e., that the honest 
sufferer from pithiatic deafness and the malingerer have this point of simi¬ 
larity—they both possess greater hearing power than their reactions to the 
older classical hearing tests demonstrate. Therefore, certain tests which are 
designed, or at least employed, to trap the malingerer may be equally 
essential and useful in establishing a correct diagnosis in the case of the pith¬ 
iatic. The two tests upon which most reliance is placed are the Lombard test 
and the cochleo-palpebral test (Gault). 

With Lombard’s test most aurists are familiar. The pithiatic obsessed 
with the idea that one ear is absolutely deaf, or that his auditory function 
is lessened to a degree greater than the actual impairment, is tested as 
follows. A noise apparatus, preferably Bafany’s, is adjusted to the sound 
ear and set in action to accustom him to its sound. He is then asked to 
recite or, if he is not illiterate, to read aloud from a printed page. He is in¬ 
structed not to stop reading when the noise instrument is placed in action. 
While he is reading aloud, the machinery of the noise apparatus, the ear¬ 
piece of which occludes his sound ear, is started. If the hearing of the 
opposite, supposedly diseased, ear is impaired, he will immediately speak 
in louder tones; if it is absolutely deaf, he may actually shout. If he con¬ 
tinues to read in an even tone or with only slight elevation, we know that 
the deafness or impairment is not real. The test is based on the fact that 
the normal individual depends upon his perception of his own voice sound 
for the regulation of its tone and intensity. 

Gault’s cochleo-palpebral test is a utilization of the fact that a normal 
person, if an unexpected sound is suddenly heard near either ear, will con¬ 
tract the orbicularis palpebrarum of the eye nearest the source of sound. 
The patient is seated, the sound ear is tightly closed with a finger, and an 
assistant of the examiner, standing behind the patient, suddenly produces 
some mechanical sound not loud enough to impress the closed (sound) ear. 
It can be appreciated, therefore, only by the ear under investigation. If 
heard, there will be a noticeable contraction, or winking movement, of the 
corresponding eye; and conversely from this winking movement, however 
slight, we have reliable evidence that the sound has been heard by the sup¬ 
posedly diseased ear. 

These are the two tests which have apparently been most useful in the 
diagnosis of difficult cases of pithiatic deafness. Naturally if malingering 
is suspected, all the available tests for intentional simulation will be em¬ 
ployed (see tests for malingering, page 96). 

A complete statement of the routine methods of examination and of the 
treatment of these patients, even if the writer were competent to present it, 
the space at his disposal will not admit of here. That there are many per¬ 
fectly honest pithiatics— i.e., sufferers from psychic deafness in whose dis- 

35 


546 


OTOLOGIC LESSONS OF THE WORLD WAR 


orders malingering plays absolutely no part—is proved by the statements of 
distinguished otologists as to the ready and remarkably rapid response of 
many of these unfortunates to skilful treatment. And this treatment is 
not by the brow-beating tactics which might logically, but in the writer’s 
opinion never wisely, be utilized to convict an obvious malingerer. On the 
contrary, it calls for the use of tact in the effort, not to accuse, but by the 
employment of established methods of encouragement and suggestion to 
efface an obsession and thereby awaken hope. As illustrating the absence 
of harshness in the rationale of treatment, a single instance may suffice:— 
to a patient tested by Lombard’s or Gault’s method a positive reaction to 
either of these tests is presented not as evidence that he has deceived him¬ 
self and his physicians, but as an encouraging sign of an intact perceptive 
mechanism,—a fortunate fact upon which both he and his physician may 
base their hope of ultimate improvement or recovery. 

Stress is laid on the fact that routine use of ordinary local methods of 
treatment, e.g., inflation, etc., is unwise for the double reason that (a) they 
may do harm and (b) lack of favorable results appreciable to the patient 
may react unfavorably upon him. 

Occasional use of certain auditory exercises, care being taken to select 
sounds he is known to hear with comparative ease, is advised, not for any 
expected influence on his actual hearing power, but for their influence upon 
his morale, and with a view to stimulating his will to hear. 

In conclusion the writer wishes to acknowledge his indebtedness to the 
admirable and interesting book, War Otitis and War Deafness, by Doctors 
Bourgeois and Sourdille, which has supplied most of the material for this 
chapter. If frequent references to it have been absent from his pages, that 
omission has been solely in the interest of brevity, and with this inclusive 
statement in mind. 

For the convenience of readers, we append below a short list of papers 
bearing upon the subject matter which we have attempted in this chapter 
briefly to outline. 

L L’organe de l’audition, pendant le guerre: Labyrinthisme, examen 
fonctionnel. Prof. E. J. Moure et P. Pietri. Archives de Medicine et de 
pharmacie militaires. Vol. 65, Pp. 809-837. 

2. L'organe de l’audition pendant le guerre: Le sourd cerebral, l’exa- 
gerateur, le simulateur. Prof. E. J. Moure et P. Pietri. Revue de laryn- 
gologie, d’otologie et de rhinologi, Vol. 38. Pp. 185-208. 

3. Recherches experimentales et histologiques sur la commotion des 
labyrinthes. Prof. Prenant et le Dr. A. Castex. Abstracted in Revue de 
Laryn, etc. Vol. 38. P. 427. 

4. Paralyses faciales de la guerre. Prof. E. J. Moure; Presse Medicale, 
April 13, 1916. 

5. Blessures du conduit auditif externe. Dr. J. Rozier. Revue de Laryng., 
d’otol. et de Rhin., vol. 38, Pp. 361-374: 384-400. 

6. Etude sur les traumatismes de l’appareil auditif. Dr. H. Abrand* 
Revue de Laryn. etc. vol. 38. Pp. 433-447. 457-467. 


GAULT'S COCHLEO-PALPEBRAL TEST 


547 


7. Morbid Anatomy of War Injuries of the Ear: Drs. J. S. and John 
Fraser, Journal of Laryngology, Otology and Rhinology. Pp. 340-353. 
369-385. 

8. War Deafness with Special Reference to the Value of the Vestibular 
Tests: Drs. P. McBride and A. L. Turner: Lancet, July 20, 1918. 

9. Effects of High Explosives on the Ear: J. Gordon Wilson, British 
Medical Journal, Mar. 17, 1917. 

10. Further Report on the Effects of High Explosives on the Ear: 
J. Gordon Wilson: British Medical Journal. May 5, 1917. 

11. Effects of High Explosives on the Ear: J. Gordon Wilson, N.'Y. 
Medical Journal, February 23, 1918. 


CHAPTER XXIII. 


SALVARSAN IN THE TREATMENT OF AURAL DISEASE. AUDITORY 
NERVE LESIONS OCCASIONALLY FOLLOWING 

ITS USE. 

Syphilitic lesions of the middle ear are in many cases more difficult 
of accurate diagnosis than in any other part of the body. It is evident 
that a specific ulcer at the pharyngeal mouth of the tube may spread 
through the canal to the tympanum. If a syphilitic ulcer within the tym¬ 
panum spreads outward through the external auditory canal, there may 
result a destruction of tissue so characteristic as to suggest per se the etio- 
logic basis of the lesion. Frequently, however, such extension does not 
take place, the lesion remaining confined within the tympanic spaces and 
assuming early the character of a chronic middle-ear suppuration of 
offensive and most intractable type. If the physician has failed to obtain 
a history of syphilitic infection and his suspicion has not been aroused 
by other manifestations of the disease, he may remain in ignorance of the 
character of the aural lesion. And yet the uselessness in such a case of 
any form of local treatment which is not combined with constitutional 
remedies must be obvious. The writer is inclined to believe that such 
negligence is not so rare as it should be. 

As the tympanum, and in fact any part of the sound-conducting 
apparatus, may be attacked by the syphilitic virus, so also, though with 
less frequency, the auditory labyrinths or auditory nerves may become 
involved. 

There is no question that the introduction of salvarsan has resulted 
in a world-wide renewal of interest in the study of syphilis in all its various 
phases. This has led not only to the establishment of certain facts in 
regard to the influence and value of the drug in question, but also to a clearer 
knowledge of many phases of the disease itself. For example, the analysis 
of a large series of cases compiled from the clinical records of institutions in 
various parts of the world has thrown a stronger light than has ever before 
been shed upon the cranial-nerve lesions occasionally resulting from 
syphilis. Seen thus in the aggregate, the number of such nerve lesions 
has reached a total sufficiently large to be impressive. Under this stim¬ 
ulus for further investigation, it is probable that in many cases cranial 
nerve disease has been observed and duly chronicled which formerly might 
have escaped notice, or at least might not have been recorded. 

It has been found that certain cases of syphilis treated by salvarsan 
have developed cranial-nerve lesions, and that, of the nerves involved, 
the eighth pair has been more frequently attacked than any of the others. 
It has been stated further that under treatment by arsenobenzol (“606”) 
a larger number of cranial-nerve lesions have occurred during the early 
548 


AUDITORY NERVE LESIONS DUE TO SYPHILIS 549 


stages of syphilis than would appear from earlier records to have resulted 
from the older methods of treatment. Arguing from these premises, it 
has been assumed by some observers that the drug itself, rather than the 
syphilitic virus, has been responsible for the lesions of the optic and audi¬ 
tory nerves occurring during the early stage of the disease. Logical as this 
deduction would at first seem, it is one to which the facts, as they accumu¬ 
late, seem less and less definitely to point. 

Cranial-nerve Lesions following the Use of Salvarsan.— 
J. Benario 1 (Frankfort-am-Main) has collected from the literature 14,000 
cases of syphilis treated by salvarsan, which he investigated with special 
reference to the frequency and type of cranial-nerve involvement. The 
results of his analysis, which are both interesting and instructive, may be 
stated as follows: 

In the 14,000 cases the use of salvarsan was followed by severe dis¬ 
turbance of one or other of the cranial nerves in 126 cases, or 1 in every 
111 cases. Of these cranial-nerve lesions the auditory nerve was most fre¬ 
quently involved (occurring in 62 cases), while the optic nerve (41 cases) 
came next in vulnerability. 

Comparing the total number of auditory-nerve lesions following sal¬ 
varsan injections (62 cases) with the total number of cases of salvarsan 
administration analyzed by Benario (14,000 cases), we find that the 
auditory nerve was involved once in every 226 cases treated. This per¬ 
centage, if substantiated by further observations, is so small that it should 
not be allowed to weigh heavily against the enormous advantages which 
the drug in other respects seems to possess over the older remedies. 

Pursuing his analysis yet further, Benario found that of the 126 cases 
of cranial-nerve lesions following salvarsan, 118 occurred in cases treated 
during the primary and early secondary stages, and only 8 in cases treated 
during the tertiary stage. 

Of the 62 cases of auditory-nerve disease, 11 were accompanied by 
syphilitic involvement of other nerves. This leaves 51 cases in which the 
auditory nerves bore the brunt of the attack. Of these 51 cases, the coch¬ 
lear branch alone was involved in 29, the vestibular branch alone in 5, 
and both branches in 17 cases. 

In the 126 cases reported upon, evidences of a nerve lesion occurred 
in 96 per cent, of cases within 4 months from the administration of sal¬ 
varsan, and 40 per cent, during the second month. 

Ehrlich’s explanation or theory in regard to the causation of these 
lesions is that they are due to the administration of salvarsan in insuffi¬ 
cient doses,— i.e.j doses which have been large enough to control the general 
manifestations of the disease, but which have failed to devitalize certain 
isolated groups of spirochsetse lodged in the cranial-nerve sheaths; and that 
the activity of these neglected spirochsetse gave rise to a perineuritis. 


1 Benario: Zur Statistik und Therapie der Neurorezidive unter Salvarsanbehand- 
lung, Munch, med. Woch., vol. 58, No. 14, p. 732. 




550 


SALVARSAN TREATMENT OF AURAL DISEASE 


Benario, Desneux, and Dujardin all accept the conclusion of Ehrlich 
that these nerve lesions are properly to be regarded as resulting from the 
syphilitic poison, and not directly from the salvarsan administered. To 
the support of this view Benario brings the following facts: 

1 . The long interval frequently intervening between the injection of 
salvarsan and the manifestation of cranial-nerve involvement. 

2. The nature of the pathological process itself, which, as is particu¬ 
larly evident in the lesions of the optic nerve, exhibits the characteristic 
features of an irritative or inflammatory lesion (Schantz, Tobias), rather 
than those of nerve atrophy, which is the lesion usually observed as a 
result of poisoning by other arsenical preparations. 

3. That the disease (i.e., nerve lesion) occurs almost exclusively dur¬ 
ing a fixed period of the disease. 

4. That, so far as is yet known, such nerve lesions are not observed 
in diseases non-syphilitic in origin, following treatment by salvarsan. 

5. The curability of such nerve lesions by antisyphilitic remedies, 
and particularly by salvarsan injections. 

6 . That such nerve lesions have usually followed the administration 
of small doses of salvarsan. 

7. That exactly the same manifestations have occurred under treat¬ 
ment by mercury. 

Benario believes that the exciting cause is in certain cases to be found 
not in the chemical action of the drug, but rather in failure to maintain 
complete sterility (i.e., employment of a solution not wholly sterile). 

Dr. Duel, of New York, who carefully reviewed the literature of the 
subject up to 1911, contributed to the volume of “ Progressive Medicine ” 
for that year a short but instructive resume of the work so far accomplished. 
As to the deductions to be drawn therefrom, Duel believes, with the authors 
above cited, that the auditory-nerve lesions following the administration of 
“606” are usually to be interpreted as manifestations of the disease, and 
not as accidents resulting from the injections of arsenobenzol. 

As contrasting with the above conclusions, the views of Prof. Alex¬ 
ander, 2 of Vienna, are of interest. Alexander’s contribution to the subject 
is based upon a careful clinical study of cases referred for aural examination 
from the dermatological clinics of the Vienna General Hospital and the 
Vienna Polyclinic Hospital prior to 1910. During this time he had ob¬ 
served 68 cases of syphilitic disease of the ear. Only 9 of these had been 
indubitable cases of syphilitic involvement of the auditory nerve occurring 
in the early stages of syphilis. Of these 9 cases, 4 were of very slight and 
transient involvement, all symptoms rapidly disappearing under mercurial 
treatment. This left therefore only 5 cases of serious syphilitic involve¬ 
ment of the auditory nerve occurring in the early stages of the disease 
during a period of six years. Yet Prof. Finger had seen 3 such cases within 


2 Alexander: Possible Effects upon the Auditory Labyrinth of the Ehrlich-Hata 
Remedy, Annals of Otology, vol. xx, No. 2, pp. 441-9. 



AUDITORY NERVE LESIONS DUE TO SYPHILIS 


551 


a period of six months. The 3 cases of Prof. Finger had been of patients 
treated by salvarsan. The 5 cases of Alexander were of patients treated 
by the older method,— i.e., mercurial inunctions, etc. Alexander, there¬ 
fore, concludes that the increased frequency of auditory-nerve involvement 
as shown in Finger’s cases is in some way related etiologically to the use 
of salvarsan. Referring to the previous literature, Alexander calls atten¬ 
tion to the great rarity of syphilitic disease of the auditory nerve during 
the early stages of the disease prior to the introduction of salvarsan. 

Summing up his personal deductions, Alexander believes (1) that, 
when acute or chronic disease of the auditory nerve or labyrinth is present 
in the early stages of syphilis,—whether the auditory-nerve lesion be 
syphilitic or non-syphilitic,—salvarsan is a dangerous drug and should 
not be administered; (2) that in the tertiary stage of syphilis or chronic or 
latent syphilis, the occurrence of an acute affection of the auditory nerve 
should be regarded as a contra-indication to the use of salvarsan; (3) on 
the other hand, there are a large number of cases of chronic syphilitic 
involvement of the auditory nerve and chronic labyrinthitis complicat¬ 
ing chronic syphilis in which he regards salvarsan as a safe and valuable 
remedy. 

The above conclusions are of interest and are worthy of careful con¬ 
sideration. They can not, however, be accepted as reliable guides to 
treatment, for the reason that the interpretation of clinical facts, upon 
which they are based, is open to question. 

For example, Alexander’s views are based upon his belief that the 
occurrence of cranial-nerve lesions during the early stages of syphilis is 
a development dating chiefly from the introduction of salvarsan. Even 
should this fact be susceptible of proof,—which apparently it is not, 
further investigation would still be necessary in order to determine whether 
the increased frequency of such “ neuro-recurrences is due to the chemical 
action of the drug itself or to some factor depending upon a faulty method 
of administration. 

Benario 3 has analyzed 29 cases of cranial-nerve lesion in syphilis 
treated by injections of mercury. Ten of these were lesions of the auditory 
nerves, in all of which the evidences of nerve involvement followed the 
mercurial injections. Of this series of 10 cases, in 8 the deafness following 
mercurial injections was relieved by injections of salvarsan. The restora¬ 
tion of function following salvarsan injections was partial in two cases, 
complete in six cases. In one case the symptoms of auditory-nerve in¬ 
volvement disappeared under further mercurial treatment. In the remain¬ 
ing case the deafness following treatment by mercurial injections was not 
relieved by subsequent injections of arsenobenzol. It would seem, there¬ 
fore, that cases of syphilis treated by injections of mercury and cases 
treated by injections of salvarsan are alike subject to cranial-nerve lesions. 


3 Benario: Ueber syphilitische Neurorezidive in besondere solche nach Quecksil- 
berbehandlung, Munch, raed. Woch., vol. 58, No. 1, p. 20. 







552 


SALVARSAN TREATMENT OF AURAL DISEASE 


Fordyce believes that, when in any considerable series of cases treated 
by salvarsan the number of cranial-nerve lesions reaches an unusually 
high percentage, the possibility of a faulty technic should be considered. 
In support of this view, he calls attention to the fact that these nerve 
lesions were far more common during the earlier experiences with the drug, 
— i.e., before the importance of using only freshly prepared solutions, 
made with freshly distilled water, was appreciated, and during the time 
when the drug was administered in doses now generally recognized as 
having been insufficient. 

Referring to Professor Finger’s report as to the frequency of cranial- 
nerve lesions following the administration of salvarsan, a comparison of 
his reported ratio with that of others, cited below, furnishes food for 
thought: 


Finger, Vienna. 500 cases; cranial-nerve lesions, 44 

Wechselmann, Berlin.2800 cases; cranial-nerve lesions, 10 

Arning, Hamburg.1000 cases; cranial-nerve lesions, 2 

Schreiber, Heidelberg.1060 cases; cranial-nerve lesions, 1 

Fordyce, New York. 800 cases; cranial-nerve lesions, 1 


In the light of Yakimouf’s experiments, proving that salvarsan solu- ' 
tions may carry active pathogenic bacteria, and Ehrlich’s warning as to 
the necessity of using only fresh solutions of the drug made with freshly 
distilled water, so disproportionately large a percentage of cranial-nerve 
lesions as are reported by Professor Finger, forces one to consider the pos¬ 
sibility, of some error either in his method of preparing the solution or in 
the method of its administration. 

The Use of Salvarsan .—The most optimistic view at any time held as 
to the possibilities of salvarsan was that by its use we might in favorable 
cases be able to destroy all the spirochsetse in the infected subject by a 
single dose. To render this possible, even in the most favorable phase of 
the disease, it is necessary that the drug be administered in large doses 
and intravenously. Small doses, failing to devitalize all the germs, do not 
terminate the disease, and, therefore, pave the way for recurrence of 
symptoms. Interstitial injections are so slowly absorbed that the full 
strength of the dose does not impress the organism at the same moment, 
the gradual absorption not only preventing the simultaneous neutraliza¬ 
tion of all the spirochsetae in the body, but having the further disadvantage 
that it allows time for the gradual development of immunity on the part 
of those spirochaetse which escape the early influence of the drug, so that 
subsequent doses, even though large, are less effective in eliminating the 
disease. 

While complete elimination of the poison as the result of a single dose 
remains a possibility, this happy result is so seldom attained that we have 
learned through experience a more rational use of the remedy. Since the 
so-called intensive plan of treatment has been introduced, and particu¬ 
larly since the wisdom of combining the use of salvarsan with that of 
mercury has gained recognition, the results have been far more satisfactory. 









VALUE OF SALVAKSAN IN AUEAL DISEASE 


553 


As to the practical application of salvarsan to the cure of syphilis, 
a condensed statement of some of the conclusions of Dr. John A. Fordyce, 
than whom probably no man in America has had a larger experience, 
should be of value. His plan of administration is to give first what he 
now regards as a moderate dose,— i.e., gm. 0.3 to a woman or gm. 0.4 to 
a man,—to test the patient’s tolerance of, or idiosyncrasy against, the 
drug. No contra-indications arising, this is followed within one week by 
a second injection of gm. 0.4 or gm. 0.5, according to sex. It is generally 
advisable in early cases of the infection, if no contra-indications are present, 
to give from five to six injections of salvarsan at weekly intervals followed 
by a course of mercurial injections or inunctions. If, after a month or 
six weeks of rest, the Wassermann reaction continues positive the same 
procedure may be repeated. 

Summing up his observations of therapeutic results, Fordyce says: 
“Since the adoption of an intensive and combined plan of treatment, I 
have noted no relapses whatever in about 200 patients treated in the early 

stage of syphilis.” . 

As to the cranial-nerve lesions following the administration ol salvar¬ 
san, Fordyce states that in a series of between 800 and 900 cases there has 
developed not a single lesion of the auditory nerve and only one of the 
optic nerve. In this case unilateral optic neuritis occurred m the early 
secondary stage, and six weeks after the administration of salvarsan. 

As to the curative influence of salvarsan upon pre-existing lesions o 
the optic nerve, Fordyce states his belief that it neither cures nor acceler¬ 
ates optic atrophy, but that it does exert a distinctly favorable influence 
upon optic neuritis coming on during the early period of syphilis. II this 
observation is correct, there is no apparent reason why the same may not 


be true of lesions of the auditory nerve. 

The great importance of carefully sifting the facts, and giving o con 

tradictory theories their proper values, is made clear by a comparison o 
the following views: Alexander, of Vienna, from his observations of aura 
lesions following the administration of salvarsan, concludes that salvarsan 
should not be given in the early stages of syphilis m the presence of a la >y- 
rinthine disorder of any grade or type. Fordyce, from his observation of 
the influence of the drug in clearing the system of the syphilitic poison, 
states his belief that it is in the early stages of the disease that the drug 
is most surely curative. Shall we deprive the patient of the advantages 
of salvarsan during the stage of the disease presumably most susceptible 
to its hifluence on account of a doubtful hypothesis that its use predis¬ 
poses the patient to syphilitic involvement of one or more of the cranial 

nerves? 


i 


CHAPTER XXIV. 


VACCINE THERAPY IN THE TREATMENT OF AURAL DISEASE: 

AUTOGENOUS VACCINES; BACTERICIDAL SERA 

That serum treatment in some form will continue to play an important 
role in the control of disease, there can be no doubt. While its field of useful¬ 
ness in certain forms of aural disease has been made the subject of many 
interesting papers, it cannot be said that the clinical experiences of different 
investigators or in different institutions have been sufficiently uniform to 
bring universal recognition of its value. There is need of further investi¬ 
gation in order to determine more definitely its field of usefulness and its 
limitations. 

In venturing to touch upon this important subject the author will 
not attempt more than to state briefly the rationale of the remedies under 
consideration, and to indicate certain types of aural disease to the relief 
of which they have seemed to contribute. 

Preliminary Remarks. —In the first place, it must be remembered 
that the pneumococci, streptococci, staphylococci, and other germs usually 
associated with aural suppuration are of the class of bacteria which have 
the property of elaborating within themselves certain toxic substances 
known as endotoxins. The endotoxins of this class of bacteria are not 
yielded readily to the circulating fluids of the body, being set free only 
with the death or approaching dissolution of the parent micro-organism. 
Each particular germ produces only its own specific endotoxin, which 
differs from all the others, and is neutralized only by antibodies called into 
being by the parent germ. This is an important fact bearing particularly 
upon the therapeutic value of autogenous vaccines, and upon the frequent 
worthlessness of stock vaccines. 

The bacteria of aural suppuration do not, then, elaborate an easily 
soluble toxin which reaches the circulating fluids during their period of 
life; and they exert their morbid influences chiefly in two ways,—viz., 
(1) by the irritation caused by their physical presence within the tissues'; 
and (2) by the systemic disturbances caused by the circulation in the blood 
of the endotoxins which are set free by the death of each succeeding set 
of bacteria. 

Before considering the remedies at our disposal, let us recall briefly 
some of Nature’s weapons of defence against such bacterial invasion,— 
viz., the phagocytes, opsonins, and antibodies. 

I. The leucocytes —or, as they are commonly called in their relation 
to the control of disease, the phagocytes —have the power of actually de¬ 
stroying pathogenic bacteria. Under conditions of normal resistance, 
the development of a suppurative lesion in any part of the bodv is followed 
554 


USE OF VACCINES IN AURAL DISEASE 555 

by a migration of leucocytes to the part and, if the lesion is of sufficient 
severity to threaten systemic disturbance, by an increase in their total 
number circulating in the blood. Any increase in the number or virulence 
of the invading germs is accompanied or followed by an increase in the 
number of leucocytes, and particularly of the polymorphonuclear cells. 
If, however, the bacteria gain the ascendency, the continued call for re¬ 
inforcements may exhaust the resources of the organism, and we shall 
have the spectacle of an individual becoming progressively more septic, 
while examination of the blood shows a diminishing leucocyte count and 
a diminishing polymorphonuclear cell percentage. These, of course, are 
generally recognized clinical facts. The clinical course of the disease may, 
therefore, be regarded as to some extent a record of the changing balance 
of power between the invading bacteria and the phagocytes. 

II. Opsonins .—There exist normally in the blood certain bodies, 
called opsonins, which can not themselves destroy the bacteria, but which 
have the power of reducing their resistance, thereby rendering them vul¬ 
nerable to the attack of the phagocytes. In this way they increase the 

effective activity of the phagocytes. 

III. Antibodies. — In any suppurative lesion the presence of the 
bacteria within the tissues not only influences a migration of leucocytes 
to the part, but has also the effect of stimulating the organism to the pro¬ 
duction of certain substances known as antibodies. These antibodies 
support the phagocytes in that they either destroy or neutralize the germ 
by whose presence they have been called into existence. A fact 
which must be borne in mind is that each pus-producing micro¬ 
organism elaborates its own specific endotoxin and excites or stimulates 
the organism to the production of its own specific antibody. In other 
words, the antibody called into being by any particular genn vill 
effectively destroy or neutralize only that particular germ and its specific 
endotoxin. 

With even so brief a statement of certain of Nature’s means of combat¬ 
ing infection, we are better able to appreciate man’s attempt to turn her 
weapons into therapeutic agents under his control. 

Autogenous Vaccines .—The vaccine treatment of a suppurati\ e lesion 
is not an attempt to introduce into the system substances inimical to the 
bacteria, but rather an effort to stimulate the organism to the production 
of antibodies corresponding to the micro-organisms present. An autog¬ 
enous vaccine is prepared by cultivating the bacteria of the infection from 
pus obtained from the lesion. The bacteria thus cultivated are killed by 
subjection to a temperature of 60° C., the devitalized bacteria being sus¬ 
pended or dissolved in normal salt solution. It is found that this solution, 
iniected interstitially, subjects the patient to no risk of further infection 
but retains the power of stimulating the organism to the elaboration ot 
the corresponding antibodies. Naturally, if we can incite, the body to a 
production of antibodies potentially overbalancing the bacteria present, a 
practical immunity will be established. 


556 


VACCINE THERAPY IN AURAL DISEASE 


If we are to make intelligent use of vaccines in the control of suppura¬ 
tive lesions and to interpret correctly their results, we must bear in mind 
the following facts: 

1. The vaccine supplies nothing to the organism wherewith to destroy 
the bacteria present or to neutralize the endotoxins in the blood. It in¬ 
cites the organism to an increased production of antibodies and possibly 
of opsonins. The results, measured by clinical changes for the better, 
can not, therefore, be otherwise than gradual. Whoever expects immediate 
amelioration of symptoms is doomed to disappointment. 

2 . The use of vaccines actually places a greater tax upon the system. 
During the interval, therefore, between the first injections of the serum 
and the establishment of an increased production of antibodies, the 
condition of the patient may seem—and, for the time, actually be—less 
favorable. 

3. During the height of a severe acute suppurative lesion, the organ¬ 
ism may be taxed nearly to the limit of its resources. Under such condi¬ 
tions, the use of a vaccine might disturb the balance of power disastrously, 
producing such systemic exhaustion as to leave the bacterial poisons un¬ 
opposed. 

4. For reasons deducible from the facts stated in the foregoing para¬ 
graph, the use of a vaccine in cases of profound sepsis— i.e., in which the 
powers of resistance are already exhausted—may further deplete the 
patient’s vitality, with disastrous consequences. 

Autogenous versus “Stock” Vaccines .—The preparation of an autog¬ 
enous vaccine represents a scientific attempt to isolate from the germ 
causing the infection that part of it which stimulates the organism to the 
production of the appropriate antibodies. Its use is, therefore, an appli¬ 
cation of the principle of cause and effect. 

The stock vaccine is a similar preparation from some typical patho¬ 
genic bacterium,— e.g., a streptococcus or staphylococcus,—or from several 
strains of bacteria belonging to the same general type. Its employment 
ignores the important fact that germs of the same general type may differ 
materially in virulence and probably in other characteristics, that they 
elaborate endotoxins of different toxicity and call into being antibodies 
exhibiting like variation. If we admit as a working hypothesis that the 
antibodies called for by a streptococcus of certain grade or type are power¬ 
less to destroy or neutralize a streptococcus of a different grade, we should 
be at no loss to explain the frequent failure following the use of a stock 
vaccine. If the germ from which the stock vaccine was prepared happens 
in all respects to coincide with the micro-organism causing the infection, 
the result should be favorable. If we employ a stock vaccine made from 
a germ which is not coequal or cooperative with that of the lesion, its 
employment will not only result in failure, but will actually deplete the 
patient by placing an additional tax upon his resources,— i.e., by calling 
for the production of antibodies which are quite ineffective against the 
bacteria and endotoxins present. 


USE OF VACCINES IN AURAL DISEASE 


557 


The aural lesions which have responded most favorably to treatment 
by autogenous vaccines are the subacute and chronic types of infection, 
or those tending toward chronicity. Among these may be mentioned (a) 
subacute suppurative otitis media,— i.e., certain cases of acute purulent 
otitis media which, having passed the acute stage, obstinately resist the 
usual methods of local treatment; (b) furunculosis of the canal, the use of 
the autogenous vaccine establishing an active immunity which prevents 
the recurrences which are so characteristic of the lesion; (c) probably 
some operative cases,— e.g., following the radical operation,—in which a 
low form of tubal infection delays recovery. The above lesions, it will be 
recalled, are not those which are likely to tax to the limit the vitality and 
resources of the organism. They provide, therefore, an ideal condition 
for the establishment of an active immunity. Corroborating this view is 
the fact that the lesions mentioned are those in which the results of the 
vaccine treatment have been most satisfactory. 

Bactericidal Sera .—The use of bactericidal sera— i.e., the sera of ani¬ 
mals which have been immunized against the bacteria corresponding to 
the infection to be controlled—has not, so far as the writer knows, been 
shown to have any wide or well-defined field of usefulness in aural disease. 
Their value and place in aural therapy must, therefore, be considered 
disproved, or await further investigation. 


CHAPTER XXV. 


AURAL DISTURBANCES DUE TO DENTAL LESIONS. 

It is clear that cases properly belonging to this category are not to be re¬ 
garded as cases of aural disease. They may, therefore, be dealt with briefly. 

That individuals whose hearing is perfect and whose ears exhibit struc¬ 
turally no abnormality may suffer acutely with aural symptoms, reflexly 
induced by lesions in other parts of the body, is a fact well known to aurists. 
Thus, acute tonsillitis or cancer of the base of the tongue may give rise to 
a severe grade of earache. By far the most common cause of reflex otalgia, 
however, is dental caries. This fact is so generally appreciated by aurists 
that it is a routine practice in every aural clinic to examine the teeth of 
patients complaining .of ear pain whose ears do not show physical evi¬ 
dences of acute inflammatory disease. Very frequently the cause of the 
otalgia is clearly seen in teeth, or roots of teeth, in advanced stages of 
necrosis. In such cases the aurist is able to assure the patient that his 
suffering is not the result of aural disease, and that it will in all probability 
be relieved as soon as the carious roots have been removed or the teeth 
put in order. 

There are many cases, however, which are not so easily diagnosticated 
as the type above described. For example, the patient may complain of 
aural pain, the ears may show no physical signs of acute disease, the throat 
may appear normal, and the teeth may exhibit no evidences of disease 
which the physician is able to recognize. In such a case one may consider 
the possibility of a neuralgic or rheumatic manifestation localized in the 
ear, but such a diagnosis should not be finally accepted until the teeth 
have been examined by a competent dentist. 

A class of cases which until recent years defied correct interpretation 
is found in patients whose aural symptoms are dependent upon dental 
irregularities which even the dentist might fail to detect. These patients 
may suffer ear pain or may experience aural symptoms of less unbearable 
type. For example, some of the most perplexing and intractable cases of 
tinnitus aurium are now known to be the result of dental lesions or abnor¬ 
malities the presence of which can. not be determined except through the 
medium of a radiogram. I am inclined to believe, therefore, that every 
obscure functional disturbance of the ear— i.e., in which no rational work¬ 
ing, hypothesis can be arrived at—should be referred to a competent 
dentist with the request that an X-ray picture be secured. 

I am indebted to Dr. M. I. Schamberg, of New York, for the accom¬ 
panying radiograms showing dental lesions of patients, some of whom 
were referred to him on account of symptoms referred to the ear. Fig. 
329 shows graphically an abscess at the roots of two neighboring incisor 
teeth. In Fig. 330 the roots of a bicuspid tooth are seen projecting into the 
558 


AURAL SYMPTOMS DUE TO DENTAL LESIONS 


559 


antrum of Highmore. Fig. 331 represents the lower jaw of a patient who 
suffered from inflammation of the alveolar process and gum as a result of 
the imperfect (partial) eruption of a wisdom tooth. Figs. 332 and 333 



Fig. 329.—Radiogram show¬ 
ing abscess at roots of two in¬ 
cisor teeth. 



Fig. 330.—Radiogram: roots of a bi¬ 
cuspid tooth projecting into antrum of 
Highmore. 



Fig. 331.—Radiogram showing im¬ 
perfect (partial) eruption of wisdom 
tooth. 



Fig. 332.—Radiogram: un¬ 
erupted and abnormally placed 
tooth. 



Fig. 333. — Radiogram: unerupted 
and abnormally placed tooth. 


show unerupted and abnormally placed teeth. It is obvious that some of 
these lesions might be absolutely impossible of diagnosis except through 

the aid of a radiologist. 













560 


AURAL SYMPTOMS DUE TO DENTAL LESIONS 


The purpose of this very short chapter is to place proper emphasis 
on the two types of cases referred to,—viz., (1) those in which severe ear¬ 
ache is clearly attributable to a dental lesion the presence of which is 
easily recognized; and (2) those in which earache or more indefinite symp¬ 
toms are the result of dental abnormalities not determinable by direct 
inspection. The latter are the more important, for the reason that, unless 
a correct diagnosis is made by means of a radiogram, the patient’s symp¬ 
toms are not likely to be relieved; and, further, he may be subjected to a 
prolonged course of treatment the results of which can not be beneficial 
and may be actually harmful. 


CHAPTER XXVI. 

DEAF-MUTISM. 

The term deaf-mutism is properly applied only to the condition of 
individuals who, by reason either of congenital deafness or extreme deaf¬ 
ness acquired in the first years of life, fail to acquire or retain the power 
of articulate speech. According to these differences of origin, deaf-mutism 
is spoken of as congenital or acquired. 

Etiology. —Of the causes of congenital deaf-mutism but little is known 
beyond certain general facts relating to heredity. Owing to the frequent 
segregation of deaf-mute children in schools and institutions and the 
friendships there formed, and their clannishness in adult life, inter¬ 
marriage between deaf-mutes is exceedingly common. As to the influence 
of such unions in determining the birth of congenitally deaf children, 
the evidence furnished by statistics is less definite than one would expect 
to find it. While acquired deaf-mutism is rarely if ever transmitted, mar¬ 
riage between congenital deaf-mutes accentuates an inherited tendency, and 
the defect is more than likely to reappear in one or more of the children 
or grandchildren. On the other hand, an analysis of the family his¬ 
tories of the children attending the various institutions for the deaf 
and dumb shows that the percentage of those born of deaf-mute parents 
is much smaller than would be expected. In spite, however, of certain 
apparent contradictions, the evidence, as it accumulates, points more 
and more directly to the danger of such unions. As an extreme illustra¬ 
tion of such transmission may be mentioned the case reported by Hart¬ 
mann, in which a marriage between two congenital deaf-mutes resulted in 
the birth of four deaf-mute daughters and one normally hearing son. 
This, however, is a comparatively rare and extreme instance. 

Better illustrating the average frequency of direct transmission are 
the statistics collected by Mygge, and analyzed by Mygind, of Copen¬ 
hagen. 1 Mygge collected from the records of different countries the 
histories of 367 marriages between individuals one or both of whom were 
deaf-mutes, and found that of the children born to them 22 were congenital 
deaf-mutes,— i. e., one deaf-mute child in every sixteenth or seventeenth 
marriage. Separating these marriages further into those in which both of 
the contracting parties w'ere deaf-mutes and those in which only one was 
so afflicted, it was found that one deaf-mute child w^as born in every sixth 
or seventh marriage between two congenital deaf-mutes, whereas only 
in every thirtieth or thirty-first family in which one parent only wtis a 
deaf-mute v r as a deaf-mute child among the offspring. Naturally, taking 
all the children born of these 367 marriages, the proportion of deaf-mute 


1 Mygind: Deaf-mutism, p. 46. 
36 


561 






562 


DEAF-MUTISM 


children to those of normal hearing was much smaller, the ratio in this 
series being as 1 to 57 or 58. 

Many deaf-mutes—particularly those in whom the defect is directly 
traceable to diseases contracted after birth—are entirety without any 
history upon which an hereditary taint could be based; and the intermar¬ 
riage of two such individuals entails little if any risk of the acquired defect 
being transmitted to the children. On the other hand, congenital deaf- 
mutes whose family records include the history of many deaf and deaf- 
mute members, by intermarriage assume for their children a frightful 
risk of inherited calamity. In other words, the consensus of opinion 
among those who have investigated this subject most thoroughly (Mygind, 
Love, Bell, Hartmann) is that an inherited tendency toward deafness on 
the part of the parents carries with it greater danger for the children than 
would the severest type of acquired deafness. According to this hypothe¬ 
sis,—which is in accord with the general theory of heredity,—a marriage 
between two normally hearing individuals in both of whose families many 
deaf-mutes had been born, would be far more likely to produce deaf- 
mute children than would a union between two deaf-mutes whose deafness 
had resulted from postnatal disease. 

In investigating the family histories of deaf-mute children in Glasgow 
institutions for the deaf and dumb, Love came upon three families in 
which both father and mother were congenitally deaf. Among the chil¬ 
dren born to these three unions were five congenital deaf-mutes. Hart¬ 
mann (quoted by Love) in Berlin came across only two families in which 
both parents were deaf-mutes. In one of these the parents were congenital 
deaf-mutes, and of five children born to them four were deaf-mutes. The 
other marriage was between individuals whose deaf-mutism had been ac¬ 
quired through disease contracted after birth, and their children were 
of normal hearing. Here, then, we have a record of five marriages between 
deaf-mutes,—four congenital and giving birth collectively to nine con¬ 
genital deaf-mutes, and one between victims of acquired deaf-mutism to 
whom only normally hearing children were born. 

As further emphasizing the influence of heredity, Dr. Love cites the 
Forty-seventh Report of the Cambrian Institute, in which is given a record 
of thirty-four families in which 130 children were born, of which number 
54 were deaf. Such a record can only be explained upon a basis of heredity. 

Relation of Parental Consanguinity to the Spread of Deaf-mutism .— 
There seems to be no question that a somewhat larger percentage of deaf- 
mute children are born to marriages between blood relations than to mar¬ 
ried couples who have no blood relationship. Beyond this fact, there is 
no evidence that consanguineous marriage between absolutely normal 
individuals influences the birth of deaf-mute children. And yet there is 
little doubt that absolute and effective prevention of so-called “ cousin 
marriages” would tend in some degree to lower the birth-rate of deaf- 
mutes. Dr. J. K. Love has collected a large amount of interesting fact 
bearing upon the relation of parental consanguinity to the spread of deaf- 


INFLUENCE OF HEREDITY 


563 


mutism, among which may be mentioned the following: Among the 
Roman Catholics of Germany whose church prohibits intermarriage 
between near blood relations, the proportion of deaf-mutes to the rest of 
the Catholic population is 1 in 3000. With Protestants, by whom inter¬ 
marriage between cousins is not condemned and among whom it is by no 
means uncommon, the proportion is 1 to 2000; “ while among the Jews, 
who encourage intermarriage between blood relations, the deaf-mutes 
are as 1 to 400” (Hutchinson). 

Among authentic instances of isolated communities in which inter¬ 
marriage has flourished is mentioned the Da Souza slave colony in the 
African kingdom of Dahomey, where several generations of almost pro¬ 
miscuous intermarriage or relationship had resulted in a progeny practi¬ 
cally free from deaf-mutism or physical blemish. An even more striking 
example is the island of St. Hilda, situated far out in the Atlantic Ocean 
west from the Hebrides Islands, from which group it is as far distant as 
the latter are from the west coast of Scotland. The people of this island, 
practically cut off from active association with the rest of the world, have 
intermarried for centuries, and yet are free from deaf-mutism and other 
blemishes which such inbreeding might be expected to produce. 

In contrast with these instances is the account given by Prof. Graham 
Bell in 1880 of the hamlet of Chilmark on the island of Martha’s Vineyard, 
whose population had had little commerce with the people of the main¬ 
land, and whose families had intermarried for many generations. Among 
its population were 72 congenital deaf-mutes. 

Apparently the influence of consanguineous marriage upon the nor¬ 
mality or abnormality of the children is dependent upon the following 
conditions: In a marriage between cousins, should each be physically and 
mentally normal and free from hereditary taint, there should be little rea¬ 
son to expect other than normal children; if, however, there is in their 
family some inherited tendency toward a particular disease or physical 
defect,— e.g.j phthisis, insanity, polydactylism, deaf-mutism, or what 
not,—this inherited tendency will be intensified by their blood relation¬ 
ship, and the danger of its transmission to future generations is enor¬ 
mously increased. 

The causes of acquired deaf-mutism fall necessarily under two heads,— 
viz., lesions attacking the auditory nerve from the intracranial side (men¬ 
ingitis), and suppurative processes reaching the labyrinth by way of the 
tympanum. 

In the order of their frequency as causes of deaf-mutism may be men¬ 
tioned the following diseases: cerebrospinal meningitis, scarlatina, measles, 

diphtheria, typhoid fever, parotitis. 

Judging by the proportionate frequency of these various causes in 
the cases of acquired deaf-mutism applying for diagnosis and advice to 
the Manhattan Eye, Ear, and Throat Hospital of New York, there would 
seem to be no question that in this country more cases are the result of 
cerebrospinal meningitis than are due to any other cause. 


564 


DEAF-MUTISM 


According to Love’s investigations it would seem that meningitis 
plays a smaller role in Scotland and the British Isles generally than in 
this country or in Continental Europe. From his collected statistics 
of European countries, one is led to believe that about one-third of all 
cases are due to meningitis, one-third to scarlatina and measles, and 
the remainder to various diseases, including typhoid fever, diphtheria, 
parotitis, etc. 

While reliable statistics are not available in support of this contention, 
I am decidedly of the opinion that in New York at least one-half of all 
cases of acquired deaf-mutism are due to cerebrospinal meningitis. I 
base this belief upon my personal experience during the past ten years as 
chief of a large aural clinic in which a majority of the cases brought for 
advice on account of acquired deaf-mutism have been traceable to cerebro¬ 
spinal meningitis. 

The larger percentage of cases resulting from scarlatina and measles 
as compared with those due to other infectious diseases is explained by the 
fact—now generally recognized by those who have made a study of the 
aural complications of the acute exanthemata—that scarlet fever and 
measles more frequently give rise to severe forms of tympanic and mastoid 
suppuration than do all other infectious diseases combined. 

Parotitis (mumps) is a comparatively rare cause of acute aural disease, 
but the occasional lesions from this cause are exceedingly prone to involve 
the labyrinth and to eventuate in extreme grades of deafness—a deafness, 
which, as a rule, is permanent. 

Morbid Anatomy. —But little is learned of the pathologic basis of 
deaf-mutism from a study of living patients. It is not always possible by 
a physical examination of the ear to determine even whether the lesion is 
of congenital or acquired origin. Naturally, if it can be determined that 
the patient has never heard or spoken, and the ears present no physical 
abnormality, the inference of congenital deafness would seem justifiable. 

• Congenital deaf-mutes are not, however, immune from tympanic disease, 
and the early development of a suppurative lesion has in many recorded 
cases left the origin of- the deafness in doubt. Our real knowledge must, 
therefore, depend upon such postmortem findings as have been recorded 
and the inferences which are justifiable therefrom. 

The following lesions are mentioned as having been actually observed 
in cases of deaf-mutism coming to autopsy: (1) Bilateral absence of 
the external auditory meatus (Hartmann). It is known that this condi¬ 
tion is not infrequently accompanied by anatomical defects of the laby¬ 
rinth. (2) Absence of the modiolus, lamina spiralis, and essential struc¬ 
tures of the membranous labyrinth in the outer (i.e., apical) half or two- 
thirds of the cochlear tube. Several variations of this defect were found 
in postmortem examinations upon congenital deaf-mutes by Ibsen and 
Mackeprang, of Denmark. (3) Abnormally narrow internal auditory 
meatus; rudimentary cochlea (Romer). (4) Complete absence of both 
labyrinths and both auditory nerves (Dardel). (5) Osseous closure of 


TREATMENT OF DEAF-MUTISM 


565 


both round windows; large quantity of otoliths and colloid corpuscles in 
both saccules and in both basilar membranes (Moos). (6) Bilateral 
absence of organs of Corti with atrophy of eighth nerves (Baratoux). The 
above records of actual postmortem findings are given in Mygind’s clas¬ 
sical work on deaf-mutism, which I acknowledge as the source of these 
references. Those wishing to examine the original records of these and 
other cases of deaf-mutism coming to autopsy are referred to the admirable 
bibliography contained in Mygind’s book. 

A recent contribution to this subject is the very comprehensive review 
of the literature relating to deaf-mutism, correlated with the results of his 
own investigations, by Dr. J. S. Fraser 2 of Edinburgh, Scotland. Dr. 
Fraser holds that the terms “congenital” and “acquired” as commonly 
applied to deaf-mutism may be misleading, since even total deafness at 
birth may, as when due to intra-uterine meningitis, belong more properly 
to the category of acquired lesions. He therefore prefers to divide all cases 
into (1) those due to a developmental error or defect (which necessarily 
must be in every sense congenital); and (2) those due to concomital disease, 
e.g., meningitis, syphilis, infection, etc., whether developed in utro or after 
birth. While it is clear that there are many cases in which such a differentia¬ 
tion might be difficult or impossible, it is a suggestion which may well 
form the basis of useful and productive investigation. 

Dr. Fraser gives two case histories with postmortem findings the 
salient features of which are here included in condensed form. Case 1. A 
boy, cet. 13 years, was practically a deaf-mute from birth, although he 
apparently could hear tuning forks of 256 double vibration and higher 
up to the limit of the Hartmann set in both ears. The right drum-mem¬ 
brane was intact, while in the left ear, the drumhead was partially des¬ 
troyed and foul pus escaped from a chronically infected tympanum. As a 
result of a later extension from this focus, the patient developed a purulent 
leptomeningitis from which he died. The autopsy findings are here re¬ 
corded only as they involve the labyrinths and chiefly as to cochlear changes. 

Left Ear. —Neuro-epithelium of utricle normal but otolith membrane 
separated therefrom. Saccule collapsed and with epithelium normal only 
in parts. Duct of utricle abnormally dilated; that of saccule narrow. There 
was present a “considerable quantity of curdled lymph in the scala tyrn- 
pani. ” Corti’s organ “ is badly formed and nowhere is the normal acoustic 
papilla visible.” Membrana tectoria nowhere normal and showing in 
various parts of the coil abnormal adhesions or contacts. In contrast to 
all these abnormalities, the acoustic nerve fibres wherever present appeared 
normal and the ganglion cells were present in normal number. 

Right Ear .—Presented very similar changes. Collapsed saccule. Coch¬ 
lea duct narrow and in parts collapsed. Corti’s organ “is for the most part 
an irregular heap of cells.” “Spiral ganglion cells appear normal in num- 

2 T s Frnser: Pathological and Clinical Aspects of Deaf-mutism; Journal of Laryng. 
and OtolV, 1922,.vol. XXXVII, pp. 13 to 38; 57 to 75; 126 to 137. 




566 


DEAF-MUTISM 


ber and the hollow space of the bony spiral lamina is well filled with 
nerve fibres.” 

Here clearly was a case of congenital deaf-mutism since no acquired 
disease could have produced the changes noted. 

Case II.—This is described as a case of “ acquired or inflammatory deaf- 
mutism.” The patient, a boy of ten years, was one of twelve children, 
none of the others being deaf. He had never spoken. 

Examination: In the right ear there was a perforation in Shrapnel’s 
membrane (“attic perforation”) through which cholesteatoma could be 
seen, and pus escaped into the canal. The left drum-membrane was in¬ 
tact, though exhibiting an “adherent scar” in the upper-posterior quadrant. 

Six months after the examination recorded above, the patient developed 
a right-sided mastoiditis complicated by infective sinus thrombosis, from 
which, in spite of jugular vein ligation, he died. 

Postmortem Examination of Cochlear.—Right Side: Bony labyrinthine 
capsule normal. “There is new connective tissue and bone formation in 
the scala vestibuli, which is practically obliterated. Marked new bone 
formation is present in scala tympani in the basal coil, but in the upper coils 
the scala is practically normal. Cochlear canal is greatly dilated in all 
coils. Corti’s organ is merely a low layer of cells. ” 

Left Side: Very similar changes. Scala vestibuli filled by new con¬ 
nective tissue. Corti’s organ is “a low mound of undifferentiated cells.” 
Cochlear nerve in the modiolus is almost completely atrophied. 

Fraser says of this case that it “is undoubtedly one of acquired deaf- 
mutism resulting from (intro-uterine) suppurative labyrinthitis.” The 
grounds upon which this belief is based, though clearly stated and inter¬ 
esting, do not appeal to the author as altogether convincing. In support 
of the opposite view,— i.e., that this is a case of purely congenital origin,—• 
may be cited the following facts: (1) even a unilateral suppurative laby¬ 
rinthitis is a comparatively unusual lesion, a suppurative invasion of both 
labyrinths being exceedingly rare: (2) an intrauterine suppurative laby¬ 
rinthitis would be exceedingly difficult to determine definitely except in the 
case of a still-born child; (3) in the light of the great diversity of lesions 
established by authenticated postmortem examinations of deaf-mutes, 
there is hardly a conceivable abnormality which may not occur as a con¬ 
genital variation (see foregoing paragraph on recorded autopsy findings); 
(4) in the right cochlea there were marked hyperplastic changes in the 
basal coil of the scala tympani; but “in the upper coils the scala is practi¬ 
cally normal,” which one would hardly expect if resulting from a diffuse 
suppurative labyrinthitis; (5) the similarity of postmortem findings in the 
two labyrinths would seem to suggest in this case a developmental defect or 
error rather the result of a purulent invasion. These facts show at least 
another viewpoint, and may serve to stimulate the reader to examine for 
himself Mr. Fraser’s views as to the nature of this interesting case, and 
further to persue his scholarly discussion of the whole broad subject of 
deaf-mutism. 


TREATMENT OF DEAF-MUTISM 


567 


The pathologic changes in cases of acquired deaf-mutism show such 
lesions to consist chiefly of two main varieties: (a) Partial or complete 
destruction of the membranous labyrinth due to an infective process 
invading the labyrinth; and (b) degenerative change (atrophy) of the 
eighth nerves, secondary to meningitis. 

In view of the nature of the lesions above outlined, I cannot share 
Dr. J. Kerr Love’s optimistic view as to what may be learned of the pa¬ 
thology of deaf-mutism from physical examination of the ears of living 
patients. 

Treatment. —Deaf-mutism in the vast majority of cases is not amen¬ 
able to treatment. The only possible exceptions to this rule are found in 
cases in which islands of hearing persist which by local treatment may be 
improved to the point of bringing the patient within the category of those 
who may be taught in part at least through the ear. Ordinarily, as soon 
as deaf-mutism is positively diagnosticated, the child, having arrived at a 
suitable age, should be entrusted to trained instructors of the deaf. In 
the case of the children of the poor, the institution or school for the deaf 
and dumb at present offers the best opportunity. With the wealthy or 
well-to-do, the education of the child by specially-trained teachers, away 
from constant association with other deaf-mutes, probably gives the little 
unfortunate a better preparation for a useful and contented life. The 
statement of Dr. Hudson-Makuen, that the development of a hearing 
mother into a trained teacher, acting under and supplementing the work 
of professional teachers of the deaf, provides the ideal environment for a 
deaf-mute child, seems altogether rational. Where the mother lacks the 
inclination or will-power to play this role of love, it may be that some other 
individual may be inspired by the human need to undertake the task. 


CHAPTER XXVII. 

NASOPHARYNGEAL ADENOIDS. 

The so-called nasopharyngeal tonsil is a physiological structure. 
Only when it becomes unduly enlarged can its presence be looked upon 
as an abnormal or pathological condition. 

Normally it cannot be appreciated by inspection by reflected light nor 
does it produce any appreciable symptoms. When, however, through 
prolonged engorgement of its vessels and consequent increase of its con¬ 
nective tissue, it becomes sufficiently enlarged to produce the smallest 
degree of obstruction to nasal respiration, it must be regarded as an ab¬ 
normal condition involving many dangers to the patient’s future develop¬ 
ment and physical well-being. 

While the presence of postnasal adenoids is a condition especially 
characteristic of childhood,—increasing in size during the earlier years, 
remaining perhaps stationary from the eighth or the tenth year to puberty, 
and then gradually receding,—this is by no means an invariable sequence 
of events, the presence of large post-nasal growths in adult patients being 
not very uncommon. It is during childhood, however, that the most 
serious and permanently injurious effects of post-nasal obstruction are 
produced, and it is in childhood that their neglect by parents or family 
physician is most dearly paid for by the little patient, or, if payment is 
postponed, it hangs over him to be met, with compound interest, as he 
grows older. 

Pharyngeal adenoids in children are almost invariably accompanied 
by some degree of hypertrophy of the faucial tonsils; and, per contra, 
noticeable enlargement of the faucial tonsils is one of the most reliable 
indications of hypertrophy of the lymphoid tissue in the nasopharynx. 

Diagnosis. —Cases in which the pharyngeal growth is of such size 
and so situated as to produce very great mechanical obstruction to nasal 
respiration may present changes of facial expression so pronounced, char¬ 
acteristic, and familiar as hardly to require description. When the child 
habitually breathes through the mouth, wears a dull, listless, and somewhat 
vacant expression of countenance, presents symptoms of nasal catarrh, 
gives evidence of being either mentally behind his fellows or is hard-of- 
hearing,—with such a picture the physician’s mind at once reverts to a 
nasopharyngeal growth as the most probable of underlying causes. These 
are not the cases involving most serious risks to the child, for in the promi¬ 
nence and multiplicity of symptoms there is ample assurance of prompt 
and adequate treatment. 

Unfortunately, in only a very small percentage of cases are such pro¬ 
nounced and unmistakable physical signs present. In the great majority 
of cases the growth causes only partial obstruction to nasal respiration 
568 


NASOPHARYNGEAL ADENOIDS 


569 


and is accompanied by but few symptoms, and these not always pathog¬ 
nomonic. 

I shall not attempt to give an extended list of all the minor symptoms 
and physical signs of a nasopharyngeal growth, but shall content myself 
with stating briefly what are to me the reliable and all-sufficient indica¬ 
tions of its presence. 

(1) Inferential. —In the first place, a child under eight or ten years of 
age, with intact drum membranes, rarely becomes hard-of-hearing except 
as a result of some lesion mechanically interfering with nasal respiration. 
Pharyngeal adenoids represent by far the commonest obstructive lesion 
in children. Barring therefore labyrinth deafness, either congenital or 
acquired, impaired hearing in children is a very strong inferential sign of 
nasopharyngeal obstruction. 

(2) Retraction of Both Drum Membranes. —Physical examination of 
the ears of children suffering from adenoids will show in the vast majority 
of cases pronounced retraction of both drum-heads. The degree of retrac¬ 
tion due to this cause in children is such as is rarely seen in adult life,— 
never except in the case of extreme atrophy of the membranes. This is 
one of the most constant and reliable physical signs of postnasal obstruc¬ 
tion in children. It is present in many cases in which other indications 
are inconspicuous or absent. 

(3) Hypertrophy of the Faucial Tonsils and Presence of Granulations 
upon the Posterior Pharyngeal Wall. —Personally I have rarely, if ever, 
seen any considerable degree of hypertrophy of the faucial tonsils in a 
young child which was not accompanied by an appreciable grade of 
lymphoid hypertrophy in the nasopharynx. The presence of granula¬ 
tions along the posterior pharyngeal wall is pathognomonic of postnasal 
adenoids. The combination of these two conditions in many cases renders 
digital examination quite superfluous,— i.e., so far as determining the 
presence of adenoids is concerned. 

(4) Posterior Rhinoscopy. —The inspection of the nasopharynx by means 
of the small postnasal mirror (pages 72-73) is impracticable in the case 
of many children. In the case of children old enough or tractable enough 
to permit it, the growth will usually be seen as an obstructing mass in the 
median line, or, if of the smooth variety, presenting an apparently un¬ 
broken surface with the posterosuperior pharyngeal wall, its presence may 
be recognized by the fact that the upper portion of the posterior border of 

the nasal septum is shut off from view. 

By digital palpation the growth is recognized as a more or less soft 
mass which may be felt between the finger and posterior border of the 
nasal septum, and may also in some cases be recognized in the fossae of 

Rosenm filler. 

Treatment. —The treatment of adenoids is their surgical removal. 
There is no question that*rather harsh methods resulting in injury either 
to the pharyngeal wall or to the pharyngeal orifices of the Eustachian 
canals, or both, have in the past been more or less in vogue. The heavy 


570 


NASOPHARYNGEAL ADENOIDS 


use of a curette can remove not only lymphoid tissue but also muscle 
tissue, giving rise to cicatricial contractures permanently disturbing the 
function both of the pharyngeal mucosa and of the Eustachian canals. 

These exaggerated methods have happily of late undergone modifi¬ 
cations under a better appreciation both of the damage which may be 
wrought and of what the operation is intended to accomplish. 

Before ending this brief discussion, I wish to record my personal view 
in regard to a somewhat mooted point,—viz., the question of removing 
the tonsils and adenoids in patients suffering from acute purulent otitis 
media. There are many who still regard an acute tympanic lesion as a 
contra-indication to immediate operation. I am personally inclined to 
hold the opposite view, and to believe that, when a pharyngeal growth is 
clearly a causal factor in acute tympanic disease, the removal of the growth 
and incision of the drum membrane should be done at the same time. 
This does not mean that in every case of acute otitis media we should 
search the nasopharynx for evidences of adenoid hypertrophy, but simply 
that, when a growth in that situation may act as a hindrance to tympanic 
resolution, the acute stage of a tympanic inflammation offers a favorable 
time for its removal rather than a contra-indication thereto. In support 
of this view may be cited the following facts: 

(1) The operation of adenectomy will in a small percentage of cases 
induce an inflammatory reaction within the tympanum. It seems wiser, 
therefore, to operate during the acute stage of an existing otitis media 
when the ears can be safeguarded by free incision of the drum membranes, 
rather than wait and incur the risk of recurrence as a result of a delayed 
operation. 

(2) The free abstraction of blood from the pharynx which always 
occurs during adenectomy usually relieves tubal congestion and hastens 
tympanic resolution. 

(3) With a pharyngeal growth sufficiently large to perpetuate naso¬ 
pharyngeal congestion, recovery from acute tympanic disease is apt to 
be slow, and not in the final outcome complete. 

(4) In the experience of every aurist there are certain cases of acute 
otitis media in which all therapeutic measures fail until the nasopharynx 
is cleared of adenoid tissue. Delay in such cases means added risks. 

(5) Either myringotomy or adenectomy should be done with the 
patient under a general anaesthetic. Combining the two operations ob¬ 
viates the necessity of repeated ansesthetization. 

The Faucial Tonsils .—In the great majority of cases,—almost invari¬ 
ably in my experience,—the faucial tonsils should be removed at the same 
time as the adenoid growth in the nasopharynx. 


CHAPTER XXVIII. 

TUMORS OF THE EIGHTH CRANIAL NERVE. 

Forward. Since the present chapter represents an enlargement of the 
heretofore prescribed scope of text books on otology, a word may be said 
as to the reason for this departure from the classical arrangement. Per¬ 
haps the best excuse for the inclusion of this additional matter is the fact 
that, from the viewpoint of the needs of practical otologists, it has be¬ 
come a necessity. 

Professor Harvey Cushing of the Harvard Medical School gives the 
following data based upon the statistics of cases drawn from his own surgi¬ 
cal experience: Of 468 tumor cases, in which the lesion has been verified 
either by operation or post mortem examination, 334 were supratentorial 
and 134 subtentorial. Of the latter fifty-six were extracerebellar, and of 
these extracerebellar tumors, thirty “ arose from the nervus acousticus. ” 
Roughly speaking, therefore, 23 per cent, of all subtentorial, and 6 per 
cent, of all intracranial tumors of this series were tumors of the 8th nerve. 
These figures were taken from his monograph published in 1917. In a 
comparatively short paper published three years later, these percentages as 
a result of cases subsequently verified were increased to 24.5 per cent, and 
7. 3 per cent, respectively. 

In his more recent paper, after an allusion to the diagnostic failures of 
neurologists as compared with those of otologists, Dr. Cushing says: 
“But our mistakes, as will be seen, are more often from incorrect localiza¬ 
tion, whereas yours (i.e., of otologists) are more often due to the failure to 
recognize the presence of a tumor at all. ” This seems hardly quite fair since 
at the stage at which these patients are first seen by the aurist, and often 
for a considerable period therafter, the clinical picture is as a rule not suf¬ 
ficiently developed to bring definite and positive diagnosis within the range 
of possibility. 

Dr. Cushing is on surer ground when, after recounting in detail a number 
of case histories of patients suffering from acoustic neuromata, upon whom 
various ill-advised operations upon nasal septum, turbinates, frontal and 
ethmoid sinuses, etc., had been performed, he says: u Certainly during this 
period we can at least spare the patient from meddlesome surgery in the futile 
effort to improve the hearing.” Probably in the aggregate of oto-laryngo- 
logical practice the arraignment herein implied is not wholly unjustified. 

The author personally believes that, with the knowledge now at our 
disposal, the otologist, even though an early positive diagnosis may be, and 
usually is, impossible, should at least be able to recognize certain features 
as sufficiently characteristic of this lesion to prompt him to hold such a 
diagnosis tentatively in mind; to cause him to watch for later components 

571 


572 


TUMORS OF THE EIGHTH CRANIAL NERVE 


of the gradually developing symptom-complex, and possibly therefore to 
modify his management or treatment of such a case. 

If this view is justifiable, we reach at once the obvious corolary that the 
acquisition of a clearer and more universal knowledge of this lesion is not 
only desirable, but is actually incumbent upon all practical otologists. 

Etiology.—Of the causes of these peculiar neoplasms but little need be 
said, since so little is actually known. 

Trauma is by most observers given as the exciting cause in certain 
cases for the reason that the history of an injury to the head has been 
elicited in a certain proportion of cases. In many cases the trauma has 
antedated by many years the incidence of initial symptoms, and the causal 
relation of the accident to the nerve lesion has by no means been proven. 
In Cushing’s first thirty cases, there was a history of injuries, blows, falls, 
etc., in six, and in most of these cases the occipital region was the site of 
the injury. 

Age seems to exert no definite influence, beyond the fact that it may be 
said, in so far as recognizable symptoms are present, to be a lesion of adult 
life,— i.e., that it occurs in people of adult ages ranging from 20 to 50 or 
55 years, and is comparatively rare in old age. 

Sex seems to play no part in susceptibility to the disease, since the 
statistics based on series of cases collected from the literature by different 
observers yield opposing or contradictory results. 

Cushing quotes Sternberg, Verocay, Henschen and others, as holding 
the view, to which he also inclines, that the lesion may be regarded as of 
biologic, or embryonic, origin; or in other words, that it may represent what 
is spoken of as an “embryonic rest.” According to this view, the tumor 
results from the persistence of embryonal connective tissue, within the 
sheath of the acoustic nerve trunk. 

The tumor may involve primarily any part of the nerve trunk, the 
commoner site being the peripheral portion,— i.e., in or near the internal 
auditory meatus. 

Terminology.— Author’s Note .—There is apparently considerable con¬ 
fusion, or at least a confusing multiplicity, of names which have been 
applied to tumors of the 8th nerve. Among them we find fibrosarcoma, 
glioma, fibroma, neuroma and endothelioma as the commoner designations, 
with fibroglioma, neurofibroma and gliosarcoma as the next in frequency. 
Sarcoma, endothelial sarcoma and neuroma fasciculare are also mentioned 
by Cushing as having been applied to neoplasms presumably originating 
in the 8th nerve. The confusion, if such it may be called, arising from this 
extensive nomenclature would not be insurmountable, if it could be assumed 
that the various designations employed were indicative, or truly descrip¬ 
tive, of actual structural differences in separate and distinct types of tumor. 
A comparison of terms with the descriptions and microphotographic re¬ 
productions of neoplastic tissue accompanying different case reports, leads 
one to infer, however, that the various designations refer in many in- 


PATHOLOGY 


573 


stances not so much to actual structural differences, as to differences of 
interpretation by different observers. 

Pathology.—In their most typical form, these tumors are described as 
firm and cartilaginous in texture, rather dry and but sparsely supplied 
with blood vessels, which are almost wholly of the venous or capillary type. 

Under the microscope the most characteristic appearances are of inter¬ 
lacing fibrous bands, separated by areas of loose reticular tissue. These 
typical structures are usually well demarcated, the one from the other. 

The fibrous bands consist largely of elongated cells with oval nuclei, 
which tend strongly to an arrangement in more or less parallel lines. The 
fibrous elements have also the characteristic feature of arranging themselves 
in relatively straight or waving parallel lines (“palisade” arrangement), 
cr in whorls. According to Councilman, these bands are “in part composed 
of fine wavy fibrils; in part the fibrils are fused together, the tissue appear¬ 
ing homogeneous. ” 

Separating the fibrous portions, or bands, and usually clearly differen¬ 
tiated or demarcated therefrom, are areas of greater or less extent of loose 
reticular tissue. The reticular areas are rather scantily supplied with cells 
of round or irregular contour. The structural resemblance of this reti¬ 
cular tissue to neuroglea and the occasional detection therein of glia-like 
fibrils— i.e., fibrils closely resembling the fine processes of glia cells proper- 
give to those acoustic tumors in which the reticular tissue preponderates 
their chief point of resemblance to typical gliomata. 

The blood vessels, mainly of venous or capillary type, are particularly 
subject to hyaline degeneration. The hyaline deposition may occur both 
within and without the vessels, its most typical site being within the lumen, 
which finally is occluded. This change is said (Councilman) to be very 
commonly associated with small areas of necrosis. 

There is apparently a considerable tendency to cyst formation within 
the tumor body, and superficial or peripheral arachnoid cysts have been 
noted in many cases. 

The accompanying illustrations (Figs. 334, 335, 336), show bettei than 
any amount of descriptive text, the typical histologic or structural char¬ 
acteristics of these tumors. . 

It is clear that great variations may occur in different tumors, otherwise 

essentially the same in type, in the relative amount of fibrous and reticulai 
tissue present; and also, that a relative preponderance of either element 
might determine the designation applied to a particular growth. It is also 
conceivable that the pathologist, receiving his impression from a particular 
section or field showing chiefly fibrous tissue, might interpret a tumor as a 
“fibroma,” whereas his impression from another specimen or field ol.the 
same neoplasm, showing chiefly extensive areas of reticular tissue, might 

lead to a diagnosis of “glioma.” 

As with variations in ratio between the two types of tissue chiefly com¬ 
posing these growths, so also are there occasional variations in the disposi¬ 
tion of cells and fibres composing these tissues. Thus Cushing states that 


574 


TUMORS OF THE EIGHTH CRANIAL NERVE 



(From Cushing’s “Tumors of the Nervus Acousticus.”) 


Fig. 334.—Area of tumor showing (X 80) the characteristic architecture of the fibrous areas 

(haematoxylin eosin). 



(From Cushing’s “Tumors of the Nervus Acousticus.”) 

Fig. 335. Fig. 336. 

Figs. 335, 336. — Characteristic architecture of fibrous and reticular areas. 







TO EPITOMIZE 


575 


in certain tumors, otherwise of the typical acoustic neuroma type, the cells 
composing the fibrous areas or bands, are in certain regions massed so closely 
and in such numbers as to justify a pathological diagnosis of fibrosarcoma. 
Again, Councilman referring to the fibrous element of acoustic tumors says: 
“these bands often form whorls converging to a single point, as in spindle¬ 
cell sarcomas. ” The interesting and fortunate fact in regard to these 
observations, is that these appearances do not appear in 8th nerve tumors 
to have the same significance, as would be attached to them in tumors in 
other parts of the body. That is to say, they convey no special indication 
of malignancy. 

The difficulty in arriving at a correct pathologic interpretation and the 
importance or necessity of careful examination of more than one or two 
sections of the same growth are clearly indicated in the pathologic notes 
accompanying Dr. Cushing’s case-histories. These in many instances, 
give a first interpretation, and a later corrected “ diagnosis,” based on sub¬ 
sequent examinations. Thus in cases XVI, XIX and XX, the first inter¬ 
pretation of “glioma” was later changed to typical “acoustic neuroma.” 
CasesXandXI which were first called “fibrosarcomata” were found later 
to be merely structural variations of the usual “acoustic neuroma” type. 
In a number of Dr. Cushing’s cases, the first laboratory interpretation was 
that of “glioma.” In only one case (case XXVI) was the diagnosis of 
“undoubted glioma” allowed to stand, the basis therefor being as follows: 
“the entire basic substance is reticular, containing definite neuroglea 
fibrillse. The predominant neucleus is small and round with no circum¬ 
scribed cytoplasm ... no suggestion of fibrous tissue.” 

To Epitomize.—Two facts seem to be established with regard to tumors 
of the 8th nerve: (1) that the most characteristic type of acoustic tumor 
presents under the microscope, certain structural features which do not 
occur in tumors originating in other parts of the body; and (2) that in 
certain cases, tumors of the 8th nerve present in certain parts a structural 
resemblance to sarcoma, suggesting a malignancy which, however, does not 
appear to be borne out clinically. In other words, such cases do not appear 
to follow a particularly malignant course clinically, although all acoustic 
tumors, probably from their pressure effects upon contiguous structures in 
the so-called cerebello-pontile angle, tend regularly toward a fatal ending. 

So much for structural features of these tumors. Of much greater 
importance to otologists,—be., in their relations to the clinical picture—are 
the gross changes wrought by pressure or displacement in neighboring 

structures. 

It is clear from case histories and post-mortem reports from many 
sources, that the vast majority of 8th nerve tumors originate from the 
peripheral end of the nerve trunk, i.e., in or near the internal auditory 
meatus. Henschen was so much impressed by the almost invariable pre¬ 
sence within the meatus of a part of the tumor growth— e.g., as established 
by his own observations and the post-mortem lepoits of othei observers 
as to incline him to the belief that all acoustic tumors originate within the 


■576 


TUMORS OF THE EIGHTH CRANIAL NERVE 


meatus. Cushing states that “Alagna’s case is one of a very few in which it 
Is specifically stated that there was not the slightest projection of the tumor 
into the porus. ” He reviews the literature as to the almost invariable pre¬ 
sence within the meatus of a part of the growth, and cites cases (Virchow’s, 
Balance’s, Askanazy-Funkelstein’s, Panse’s) in which some dilatation of 
the meatus from pressure absorption had occurred. His own conclusions 
are that, while the vast majority of acoustic tumors have their origin in the 
peripheral end of the nerve trunk, and while practically all such growths in 
their later stages send projections into the internal auditory meatus, that 
space cannot be regarded as their invariable point of origin. 

As might be expected, acoustic tumors are approximately oval in con¬ 
tour in the early stages of their development, though naturally, with their 
gradual increase in bulk, they must conform somewhat to the unyielding 
angular space between the tentorium and postero-internal surface of the 
petrous bone, while internally and backward they present a nodular surface 
which bulges against the comparatively unresisting surfaces of cerebellum 
and pons. 

Influence of Tumor Upon Other Nerves .—All the cranial nerves, from the 
5th to 12th, are in close proximity to the space usually occupied by a 
fairly large acoustic tumor. While all or any of these may be subjected to 
pressure, the facial and trifacial are the two nerves which commonly suffer 
the greatest distortion. The facial trunk being always in relation to the 
upper end, or pole, of the tumor may be elongated to an extent three times 
its normal length or more. The trigeminus, which also is pressed upon by 
the uppei end of the growth, may be similarly stretched. Cushing states 
that it is a matter of wonder, the degree to which these nerves may be 
elongated, flattened and attenuated without appreciable disturbance or 
loss of function. This is the more surprising in the case of the 7th nerve 
since in addition to stretching and displacement, it must also be subjected 
to an unusual degree of pressure within the internal auditory meatus. Pro¬ 
bably this rather lemaikable retention of function in a motor nerve is to be 
explained by the very gradual development of pressure, the nerve fibres 
ha\ mg time to accommodate themselves to the gradual changes in struc¬ 
tural arrangement or relationship. Unquestionably, any like degree of 
pressure or distortion, suddenly applied, would result in immediate, and 
complete, though not necessarily permanent, paralysis of the supplied 
facial muscles. The abducens, though from its position apparently less 
subject to pressure than any of the cranial nerves mentioned, is neverthe¬ 
less paralyzed occasionally in cases of 8th nerve tumor. At their points of 
emergence from the medulla the glossopharyngeal, pneumogastric and 
spinal-accessory nerves are in fairly close relation to the 8th nerve, though 
diverging from and passing below the latter in their course toward their 
point of exit from the skull through the foramen lacerum posterius. They 
aie, theiefore, pressed upon by the lower end of an acoustic tumor and may 
undergo great elongation and distortion. 


INFLUENCE UPON INTRA-CRANIAL PRESSURE 577 


Influence of Tumor Upon Pons , Cerebellum arid Medulla. —'Naturally a 
tumor so situated as to exert direct pressure inward upon the pons, inward 
and downward upon the medulla and inward and backward upon the cere¬ 
bellum, may cause great displacement and distortion of these structures. 
Cushing states that in cases in which a wide decompression operation for 
the relief of tension has been performed, the acoustic tumor in certain in¬ 
stances reaches a size or length rarely or never seen where the skull remains 
intact; and the fact of this retardation of tumor growth as a result of its 
confined space, gives us a clear conception of the enormous pressure to 
which the cerebellar, pontile and medullary structures are themselves 
subjected. It is not surprising, therefore, that in the later stages of such a 
growth, the adjacent half of the pons may be compressed to half its normal 
size, the cerebellar hemisphere deeply impressed and even the medulla 
indented and displaced. Add to the pressure of increasing tumor bulk the 
influence of distended ventricles and the displacement of the whole brain 
stem toward the opposite side, the compression, or herniation, of cerebellar 
tissue downward toward or even into the foramen magnum and the pressure 
absorption of the petrous bone and skull plates are not incomprehensible. 

Influence of Tumor Upon Intra-cranial Pressure. —No clear or compre¬ 
hensive picture of the gradually developing symptom complex is possible 
without an intelligent consideration of the enormous increase of intra¬ 
cranial pressure to which this lesion may give rise. This increase is due 
not only to the direct influence of the increasing tumor bulk but also to 
the disturbance of free circulation of cerebral fluids with consequent ven¬ 
tricular distension. It must be borne in mind that we are considering a 
subdural growth lying, as Cushing expressed it, “ within an arachnoid cap¬ 
sule.” He calls attention to the fact that while this may be difficult of 
demonstration post mortem when the membranes have been disrupted 
during removal of the brain from the skull, it is usually quite obvious 
during operation “when the arachnoid spaces are distended with fluid.” 

Barany has described the train of symptoms due to distension of what 
he calls the cisterna pontis lateralis. This space lies in the so-called cere- 
bello-pontile angle,—or, to be more exact, is in close relation to the internal 
auditory meatus, and that portion of the postero-internal surface of the 
petrous bone immediately surrounding it. Within the lateral cistern are 
found the glossopharyngeal and vagus nerves, the lateral choroid plexus, 
and the facial, acoustic, and trigeminal nerves, all of which structures may 
suffer compression or distortion by an acoustic tumor. Baran\ assumes 
that this space, which has communications with the other ventricular 
reservoirs of the brain, may become distended through inflammatory ad¬ 
hesions between pia and arachnoid with consequent disturbance of the 
circulation of the cerebral fluids; and he describes a group of symptoms— 
nystagmus, vertigo, ataxia, loss of normal pointing reactions, etc. all of 
which may form part of the characteristic symptoms-complex of a tumor of 
the 8th nerve. If such disturbances are possible as the result of a simple 
inflammatory process, one should have little difficulty in conceiving the 

37 


578 


TUMORS OF THE EIGHTH CRANIAL NERVE 


enormous and generalized pressure changes through ventricular distension, 
which may be produced by a tumor which by direct or indirect pressure 
may close or obstruct the foramena of Luschka and Monro, and possibly 
also the aqueduct of Silvius. This degression is made here solely for the 
light it may throw upon an important factor in the symptomatology of 
this lesion. 

Symptoms. —-Cushing lays great stress upon the importance of the 
“ chronology, ” or the order in which the symptoms of an acoustic tumor 
appear; and while this important factor in the diagnosis has, so far as the 
writer knows, not been duely emphasized by other writers, the observation 
accords so logically with the histologic and gross pathology of such a lesion 
as to carry immediate conviction of its accuracy. In fact it would almost 
seem that, without any knowledge of symptoms, one might deduce that a 
slow-growing tumor originating in the trunk of a nerve of special sense 
would proclaim its presence: (1) by functional disorders of the organ sup¬ 
plied; (2) by symptoms of intracranial discomfort; (3) by symptoms in¬ 
duced by pressure upon, or displacement of, adjacent structures,— e.g., 
nerves or organs; (4) by symptoms referable to increase of intracranial 
pressure, e.g., pressure upon brain centres, more distally placed nerves, etc. 

Deafness. —Almost of necessity the first appreciable symptoms of an 
8th nerve tumor are those referable to the nerve itself, i.e., impaired hear¬ 
ing, homolateral and at first not sufficiently pronounced to alarm the patient. 
W liile qualitative analyses of the auditory defect seem to be entirely lack- 
ing, it is inconceivable that the type of impairment can be other than that 
known to otologists as “nerve deafness.” In support of this deduction is 
the recurring statement in Cushing’s case-notes that the patient’s attention 
was first directed to a loss of hearing by difficulty in using the telephone, 
which is distinctly not the case with the commoner type,— i.e., of obstruc¬ 
tive deafness. 

1 innitus aurium is also one of the usual symptoms of this early stage. 
Probably in many cases, the subjective noises represent the first indication 
of aural disorder. 

The deafness in acoustic tumors has the following characteristic fea¬ 
tures: it is of nerve or labyrinthine type; it is uninfluenced by local treat¬ 
ment; it is progressive and probably very rapidly progressive, and tends 
regularly, though with some exceptions, to complete loss of function. 

1 estibidar Disturbances. —That a lesion originating in the nerve trunk, 
and believed by some (Henschen) to involve primarily the vestibular 
branch, should produce no onset-symptoms of vestibular upset or distur¬ 
bance, would seem at first almost incredible. Case reports are so contra¬ 
dictory as to this phase of the syndrome, however, that it will be reserved 
for & brief later consideration. Undoubtedly some evidence of vestibular 
involvement must be present at the onset in the great majority of cases. 

j\ote. It may be said with approximate certainty, that deafness, 
tinnitus and possibly vertigo, are the initial symptoms in practically all 
cases ol acoustic tumor, although their importance may have impressed 


PAIN—CEREBELLAR SYMPTOMS 


579 


the patient so little, that he may have completely forgotten the date of 
their onset when the next and more alarming components of the syndrome 
make their appearance. It is this long waiting period—possibly measured 
by years—between the unspectacular onset and the further development 
of symptoms, which makes an early diagnosis so exceedingly difficult 
a problem. 

Pain .—-Next in order of sequence, and certainly representing a stage of 
tumor development very considerably later than that of the initial deafness, 
are certain subjective sensations of. distress, discomfort or actual pain in 
the head. These may take the form of inconstant and rather indefinite 
pain or may reach a degree of considerable severity. They are usually 
homolateral and occipital, or may be frontal. They may alternate between 
the occipital and frontal regions, but more often have their point of greatest 
severity and persistency in the subtentorial region with radiating or shoot¬ 
ing pains in the direction of the frontal region. They are subject to periods 
of relief or amelioration; they are usually worse at night, or may afflict 
the patient only at night, subsiding wholly in the morning or as the day 
advances. 

Naturally with a subjective symptom of such variable and, in some 
cases, intermittent type, its diagnostic value, unless supported by other 
evidences of intracranial disease, may be slight. Usually, however, other 
characteristic phenomena may be detected. With the progress of the 
lesion the head pains tend to become more definitely localized and of greater 
severity; and with their gradual accentuation, the homolateral occipital 
and neck muscles in some cases become markedly sensitive or tender,—so 
that the patient, to relieve tension, holds the head tilted somewhat to the 
affected side. 

Cerebellar Symptoms .—-As one would expect, symptoms induced by com¬ 
pression or distortion of cerebellum, pons Varolii or medulla are of later 
development than those referable to the pathologic changes in the 8th 
nerve itself. From the author’s analysis of case reports he is inclined to 
believe that they may appear at any period from 2 to 10 years after a 
correctly noted initial deafness. It must be borne in mind, however, that 
a unilateral deafness often excites little notice so that in certain cases the 
graver symptoms may appear to follow quickly upon the first appreciation 
of auditory loss. 

The chief cerebellar symptoms are: nystagmus; incoordination ataxia 
and diadokokinesis; static and dynamic ataxia. 

The nystagmus apparently varies considerably in different cases. From 
the descriptions, one receives the impression that in a majority of cases the 
direction is toward the side of the acoustic tumor, and that it becomes 
more pronounced when the eyes are rotated in that direction. 

Homolateral incoordination ataxia of the arm and leg muscles and 
homolateral diadokokinesis are almost always present. They are probably 
to be regarded as different manifestations of the same disturbance rather 
than separate symptoms. Probably homolateral paresis of the affected 


580 


TUMORS OF THE EIGHTH CRANIAL NERVE 


muscles is usually present, since this is a common concomitant of the inco¬ 
ordination ataxia and diadokokinesis of all cerebellar lesions. 

Static and Dynamic Ataxia .—The gait is markedly unsteady. The 
patient may be able in walking to pursue a straight course, but does so 
with effort and with feet well apart; or he may be quite unable to stand 
or walk, the falling direction or tendency being usually toward the side 
corresponding to the lesion. 

The tendency of the patient to fall toward the side of the lesion is pro¬ 
bably to be accounted for in one of two ways: (1) the homolateral inco¬ 
ordination, semiparesis and diadokokinesis would naturally tend, through 
the resulting lack of support and resistence, to throw his body in that 
direction; and (2) in addition to the above or, it may be, quite independ¬ 
ently, there may be an abnormal impulse, resulting perhaps from pressure 
upon, or injury to, some part of the complex mechanism of orientation,— 
basal centre, association tract or possibly a so-called direction centre in the 
cerebellar cortex (Barany), which impels the body in the given direction. 

Naturally with objective disturbances of equilibrium so pronounced, 
subjective vertigo of a distressing type is likely to be present. 

The above so-called cerebellar symptoms occur regularly at some stage 
of an acoustic tumor in the great majority of cases, and may be generally 
regarded as signifying a growth which has already attained a very consid¬ 
erable size. 

Before leaving this brief outline of cerebellar phenomena, a word may 
be said, from the otologist’s viewpoint as to the differential value and 
significance of nystagmus and ataxia as seen or reported in the course of 
this lesion. 

Nystagmus .—From the detailed reports of Dr. Cushing’s first series of 
thirty cases—unusually complete in most respects—we learn but little as 
to the nystagmus beyond the meagre fact that it is almost invariably pres¬ 
ent, its absence being noted in one case only (case vii). Such statements 
as “nystagmus, coarser excursions to right” (case ii), “nystagmus, slower 
to left” (case hr), “nystagmus, coarser to left” (case iv), etc., recur fre¬ 
quently as the only qualifying term. In only two of the thirty cases (cases 
XX and XXI) is the direction of the quick component of the nystagmus 
given. From the otologist’s viewpoint, the mention of a nystagmus in 
connection with either a labyrinthine or a brain lesion without definite 
statement or indication of the direction of its quick component, is to de¬ 
prive it of its chief diagnostic significance. Dr. Cushing’s histories are and 
should be of such interest to otologists, and the character of the nystagmus 
is from the otological viewpoint so essential to a correct interpretation of 
the accompanying phenomena of vertigo and ataxia, that it is to be re¬ 
gretted that he has not been sufficiently interested in Barany’s work on the 
labyrinth and his later work on cerebellar localization to have adopted 
terms which would convey a distinct and definite meaning to otologists and 
neurologists alike. In other words, if this lesion is to come under the 


581 


DISEASES OF THE ADJACENT NERVES 

joint study of neurologists and otologists, a code of terms intelligible to 
both is clearly essential. 

More than once in his treatise on acoustic tumors (pp. 155, 156 and 161), 
Di. Cushing speaks of the question of a vestibular or cerebellar origin of 
the chai acteiistic nystagmus and ataxia of the later stages of these neo¬ 
plasms as one often difficult of solution. \ et from the otological viewpoint 
it would seem that this question should not present great difficulties, and 
foi fhe following reasons: (1) in most of these cases the evidence of early 
paialysis of the vestibular nerve seems complete, and active nystagmus 
and ataxia from a functionally inactive vestibular nerve is almost invariably 
of short duration. In other words, in the severest types of vestibular 
lesions, e.g., suppurative labyrinthitis, the nystagmus and accompanying 
disturbances of equilibrium usually subside quite rapidly. (2) If, as Dr. 
Cushing believes, the involvement of the vestibular nerve trunk occurs in 
many cases without any onset-symptoms of vestibular disturbance, it is 
inconceivable, in the light of what is actually known of vestibular phy¬ 
siology and reactions, that such phenomena could occur as a late manifes¬ 
tation of such a lesion. (3) In any given case, spontaneous nystagmus and 
static ataxia both being present, a study ol the ataxia, i.e., relation of the 
falling direction or tendency to the direction of the quick nystagmic com¬ 
ponent, to changes in the position of the head, etc., should suffice either to 
establish or eliminate the diseased vestibular mechanism (nerve trunk or 
labyrinth) as responsible for the symptoms in question. 

Symptoms Referable to Disturbance of Adjacent Nerves .—These in the 
order of their diagnostic importance are the 5th, 7th, 6th and then the 
group of nerves (9th, 10th and 11th), leaving the skull through the foramen 
lacerum posterius. 

The 5th, or trigeminal, nerve is given precedence over the 7th, for the 
reason that the symptoms referable thereto, on account of their subjective 
character, are more surely brought to the physician’s attention and there¬ 
fore less likely to escape notice. 

Fifth Nerve .—The trigeminal symptoms are chiefly sensory, consisting 
in their most characteristic form of a parsesthesia,—usually a sensation of 
numbness, or in some cases of numbness and tingling combined—in the 
entire trigeminal area of the anterior and antero-lateral surfaces of the 
head and face. Closely associated with these sensory pervertions in the 
skin is a loss or diminution of the corneal reflex, which is perhaps the com¬ 
monest manifestation of trigeminal involvement in cases of acoustic tumor. 
Cushing instances the fact that in four cases of his series areflexa cornealis 
supplied the only evidence that the 5th nerve was involved, and in one 
case it was the only indication that any cranial nerve, other than the 
auditory nerve itself, was in any way affected. 

It will be seen from the above that the typical symptoms of 
trigeminal disturbance present the characteristics of a nerve paralysis or 
diminution of function. The opposite phenomena of nerve irritation, or 
pain, are comparatively infrequent. Slight neuralgic symptoms have been 


582 


TUMORS OF THE EIGHTH CRANIAL NERVE 


noted in some cases. But severe neuralgia— -i.e., neuralgia of character¬ 
istic trigeminal type—-is said to be uncommon. 

While all of the sensory phenomena of 5th nerve involvement are 
typically and logically homolateral, several instances have been noted in 
which they occurred bilaterally, a condition presumably due either to 
extensive contralateral displacement of the brain stem, or quite possibly 
in some cases to the pressure of the coincident hydrocephalus. 

Seventh Nerve .—'That the facial nerve, subject as it usually is not only 
to stretching and attenuation, but also to compression within the internal 
auditory meatus (see pathological notes), should not induce earlier and 
more pronounced signs of paralysis, affords a graphic illustration of the 
extensive changes which may occur in a motor nerve—provided these 
changes are gradual in their development—without complete ablation 
of function. 

While some facial paresis, shown by slight loss of motor activity and 
diminished clearness in the facial lines, is almost always present, it may be 
so slight as to pass unnoticed unless looked for, and complete facial paralysis 
is said to be exceedingly rare. 

More conspicuous, when they are present, are facial nerve disturbances 
of the opposite or irritative type. Facial twitching, or spasms, have been 
recorded by several historians of acoustic tumor cases. As compared with 
the paraesthetic type of phenomena, however, they are extremely rare. 

Sixth Nerve .—W hile the abducens is a comparatively deep-seated nerve, 
passing almost directly forward from its superficial origin to its distri¬ 
bution to the external rectus occuli, it is to some extent involved in a very 
considerable proportion of acoustic tumor cases. That the involvement of 
this nerve is said in most cases to be indicated only by occasional or inter¬ 
mittent diplopia, and that it has occurred in a number of cases bilaterally, 
seem to the writer to indicate that abducens phenomena may occur chiefly 
as a manifestation of changing conditions of ventricular pressure,—possibly 
of intermittent distension of the cistern® pontis lateral®. 

Nmth, Tenth , Eleventh a?id Twelfth Nerves .—-While all of these nerves 
undergo almost inevitably a considerable degree of elongation or stretching 
through displacement by the lower part of a fairly large acoustic tumor, 
it is probable that complete paralysis, or loss of function, is quite unusual. 
Even did actual paralysis occur, the resulting symptoms might be difficult 
to differentiate definitely with regard to their actual causes. Thus with the 
subjective disturbances of taste, not only the glosso-pharyngeal but also 
the facial, through its chorda tympani branch, would have to be considered; 
while marked pulse and respiratory changes might be due either to dis¬ 
turbance of the pneumogastric or to pressure changes affecting medulla. 
Again, the speech defects which are so commonly present among the 
symptoms of the later stage, may be due in part to involvement of the 
motor fibres of the glossopharyngeal, of the inferior laryngeal branch of 
the vagus, and possibly of certain motor fibres of the spinal accessory sup¬ 
plied to the larynx. To which of these nerves the difficulty in swallowing is 


GENERAL PRESSURE SYMPTOMS 


583 


chiefly to be ascribed is probably a matter largely of conjecture. For diag¬ 
nostic purposes, therefore, it seems better to describe all these symptoms as 
belonging to a group probably or possibly having a composite origin. They 
may be mentioned in the following somewhat arbitrary order: difficulties in 
swallowing; speech defects —usually slow, labored articulation; incontrollable 
and frequent yawning; occasional paroxysmal attacks of difficult or labored 
breathing. Probably all of these symptoms are present at some stage of the 
development of almost all acoustic neuromata. The dysphagia and dis¬ 
turbances of articulation are said to be prominent and almost invariable 
phenomena of the later stages of the disease. 

A symptom described as occasionally present is the deflection of the 
protruded tongue toward the side of the lesion. It is ascribed to involve¬ 
ment of the hypoglossal nerve. 

General Pressure Symptoms. —-Under this head must be mentioned an 
exceedingly important symptom, which seems to be one of the most un¬ 
failing manifestations of the hydrocephalus which usually marks the later 
stages of an acoustic tumor—viz., failing vision with choked disc, and pos¬ 
sibly beginning optic atrophy. The first indications of failing sight in a 
patient presenting other characteristic phenomena of an acoustic neoplasm 
are of the greatest importance, not only for their diagnostic value, but also 
as indicating a stage of the lesion when surgical intervention must not be 
unduely delayed if the patient’s sight is to be preserved. Dr. Cushing cites 
at least one instance of permanent blindness in a patient who presented 
typical symptoms of an acoustic tumor, whose sight might have been 
saved by timely surgical intervention, but who was subjected to illogical 
and futile treatment based on a false diagnosis. 

Epitome. —The symptoms of an acoustic tumor constitute a gradually 
developing symptom-complex the usual sequence of which is as follows: 
(a) homolateral impairment or loss of hearing, probably accompanied by 
symptoms of vestibular disturbance; (b) head pain or discomfort; if 
pain, usually occipital, frontal or alternating;tinnitus aurium; (c) cerebellar 
nystagmus; incoordination ataxia and diadokokinesis; static and dynamic 
ataxia; (d) paraesthesia—numbness or tingling of trigeminal region of face 
and head; areflexa cornealis; slight facial paresis; diplopia occasional or 
intermittent; all symptoms of this group homolateral, (e) Failing vision, 
with choked disc, leading to optic atrophy; (f) dysphagia; motor speech 
defects; severe paroxysmal head pains; mental and dispositional changes; 
attacks of difficult respiration; pulse changes; terminal stupor or coma. 

Since the otologist faces a peculiarly difficult problem in regard to these 
tumors, there are two points in the clinical picture which call for brief dis¬ 
cussion,— d.e. (a) The question of vestibular symptoms at the onset; 
and (b) the average duration of the interval between the acoustic and the 
later cerebellar or pressure symptoms. 

Dr. Cushing’s analysis of his own carefully made case-histories dis¬ 
closes so many instances in which no experience of early disturbance of 
equilibrium or dizziness could be recalled as to raise in his mind a question 


584 


TUMORS OF THE EIGHTH CRANIAL NERVE 


as to the frequent occurrence of early vestibular symptoms. One finds it 
difficult, however, to believe that so gross a lesion of the vestibular nerve 
could occur without definite symptoms of vestibular disturbance. It is a 
point for the otologist’s observation and study. 

Interval Between Initial (Acoustic) Stage and the Later ( Cerebellar ) Stage. 
—Definite knowledge on this point— -i.e., the average interval period— 
would be not only interesting but valuable. The author has hazarded the 
statement that the secondary phenomena might appear at any time from 
2 to 10 years after the first aural symptom. Even with so large a spread, 
however, this statement is largely conjectural. It may be interesting to 
give a correlation of Dr. Cushing’s data on this point. These patients, be 
it remembered, were first seen by him when the symptom complex was com¬ 
plete. Whenever obtainable, the number of years preceding, or the date, 
when the initial auditory failure was appreciated is stated on the history 
chart. These duration periods in twenty-two cases and stated in terms of 
years are as follows: 3, 9, 5, 214 10, 3, 2, 2, 7, 2, 2, 2, 1, 4, 3, 4, 5, 1, 2J4 1, 
3, 1; average, 34S years. This would seem very conclusive but for the fact, 
known to all aurists, that patients with unilateral deafness are extremely 
apt to understate the period of its duration. There are two sources of error 
in such data, i.e., the patient’s inability to recognize the impairment until 
advanced, and errors of memory as to dates. 

Every otologist should be able to recognize an acoustic tumor when the 
syndrome is complete and the chronology of symptoms is known to him; 
but the problem of reaching even a tentative diagnosis in the earlier stages 
is a far more difficult one. 

Treatment. —In the early stages of an acoustic tumor,—the period 
of tentative diagnosis,—the real aim of treatment should be, not im¬ 
provement of hearing, but (a) maintaining the patient’s vitality on 
the best possible plane against the stress and strain of the later 
period, and (b) careful periodic examinations for detecting any later 
components of the gradually developing symptom-complex. When the 
clinical picture has reached the point where a positive diagnosis is pos¬ 
sible, the treatment becomes purely a question of surgical experience, 
judgment and method. 

A question which has been discussed, is with regard to a choice be¬ 
tween two surgical methods, or two pathways of surgical approach, for 
iamoving these tumors: i.e., (1) the wide bilateral occipital exposure 
advocated by Dr. Cushing; and (2) the more direct route through the 
C mpano-mastoid space and labyrinth, proposed by Dr. Krause. Perhaps 
the best light upon this question may be in the statement of certain facts 
relating to the two operations. 

In the first place, the mortality following the Krause, or labyrinthine, 
operation is recorded as 80 per cent. (Fraser); by the occipital exposure 
and technic of Dr. Cushing it has been reduced to 20 per cent. 

The Cushing operation provides a wide decompression area which is in 


INITIAL STAGE AND THE LATER STAGE 


585 


itself an important factor in the relief of symptoms. It leaves a closed 
wound with practically no risks of post-operative infection. 

The Krause operation involves the maximum risks of facial nerve 
injury or destruction; does not provide a sufficient exposure for the most 
careful work upon the tumor; is far inferior to the occipital operation in 
providing durable relief of tension; and leaves a wound which cannot be 
closed, can hardly be kept surgically clean, and imposes a maximum risk of 
meningeal infection. 

Dr. Cushing’s experience has lead him to the conclusion that in the 
past the very great mortality—a mortality so large as almost to dis¬ 
courage surgical effort—has been due in part to the very natural desire and 
effort on the part of surgeons to remove these tumors in toto — i.e., with 
their capsules. The percentage of mortality in his own early experiences led 
him to substitute for the effort at capsular enucleation, a subcapsular oper¬ 
ation. This, he admits, does not effect complete exterpation of the neo¬ 
plastic tissue, but provides practical relief of symptoms over a considerable 
period. It is obviously better in any series of 100 cases, to confer an ex¬ 
tension of life with comfort upon eighty, rather than a permanent result 
upon twenty of the series at the expense of the sixty whose lives are sacri¬ 
ficed to the more radical procedure. It must be borne in mind that the 
operative procedure developed by Dr. Cushing confers an average exten¬ 
sion of life estimated at six or seven years and this without prejudice to the 
chances of relief from a second operation, should this be indicated later. 

Henschen estimated the average period of development of acoustic 
nerve tumors—presumably from the initial recognizable symptom to the 
fully developed symptom-complex—at 3^ years. This coincides with 
Cushing’s computation that from the initial symptom the patient has 
before him a period of failing health of approximately 3^ years to the 
stage where operation becomes a positive necessity. Following a successful 
operation he may expect a period of 3 to 33>"2 years of comparative health 
and comfort, when tumor symptoms reappear, presaging a period of 
failing health and gathering symptoms of equal duration, when operation 
again becomes a necessity. 

It is estimated that a patient presenting the complete symptom-com¬ 
plex of an acoustic tumor— i.e., having reached the stage of well marked 
concomitant hydrocephalus—lives on the average less than one year. 

Before closing this chapter, the writer wishes to acknowledge his entire 
indebtedness to the writings of Dr. Cushing for practically all of the facts 
presented. Those who wish to inform themselves as to the detads of the 
surgical procedure are referred to Dr. Cushing’s work on Tumois of the 
Nervus Acousticus.” No clearer or more beautiful description of a dif¬ 
ficult surgical technic is known to the author than will be found in his 

chapter on the surgical treatment of these growths. 

Differential Diagnosis— There is a rather long list of lesions said to 
have been confused with tumors of the 8th nerve, but only three which 
need be mentioned here:—(1) cerebello-pontile tumors not originating in 


586 


TUMORS OF THE EIGHTH CRANIAL NERVE 


the 8th nerve; (2) distension of the lateral cistern from inflammatory ad¬ 
hesions between pia and arachnoid; (3) syphilis of the 8th nerve. 

Tumors of the cerebello-pontile angle not of 8th nerve origin may natur¬ 
ally give rise to all or any of the symptoms entering into the symptom- 
complex of an acoustic tumor. The chief differential sign is one of chron¬ 
ology,— -i.e., deafness is the initial symptom of 8th nerve tumors whereas it 
is one of the later manifestations of tumors arising from other structures of 
this region. In fact, deafness, which is often complete in 8th nerve tumors, 
may be slight or even unappreciable in other neoplasms—- e.g ., of cere¬ 
bellum or pons—in this region. 

Distensio?i of the dsterna pontis lateralis may present a clinical picture 
strongly suggesting an acoustic tumor. It is to be differentiated there¬ 
from by the comparatively rapid development of the complete syndrome, 
and the later and less pronounced disturbances of the auditory function. 

Syphilis of the 8th nerve gives rise to sudden and often complete homo¬ 
lateral deafness with concomitant disturbances of equilibrium,—nys¬ 
tagmus, vertigo, ataxia, loss of vestibular reactions etc. It is to be differ¬ 
entiated from an acoustic tumor by the result of a Wassermann test of the 
blood and spinal fluid, and by other signs of syphilitic infection. 

Naturally an intracerebellar tumor superficially placed in the middle 
inferior lobe may present many clinical resemblances to an acoustic tumor, 
but with the important differential point of absent or slight disturbances of 
auditory function. 

In Conclusion: Admitting, as one must, the difficulty or practical 
impossibility of a positive diagnosis in the phase of initial symptoms, what 
are the aurist’s responsibilities with regard to this lesion in the stage at 
which he alone is likely to be consulted? 

Personally, I should say that, having familiarized himself with the 
chronology of symptoms, he should consider this lesion—at least tenta¬ 
tively—in all cases of nerve deafness of unexplained origin. The vestibular 
tests should be made irrespective of the presence or absence of spontaneous 
symptoms of vestibular disturbance. He should keep the earlier of the 
secondary phenomena in mind— e.g., of 7th nerve involvement—and should 
keep the patient under periodic observation for the detection of successive 
components of the symptom-complex. He should remember that deafness 
of labyrinthine or 8th nerve type is not favorably influenced either by 
local treatment of the ear or by nasal surgery. When the clinical picture 
has reached the stage of adjacent nerve involvement and characteristic 
phenomena of cerebello-pontile disturbance or pressure, he should recognize 
the patient’s right to the best available neurological opinion and advice. 
Finally, a diagnosis having been made, he should bear in mind that the 
lesion is one calling for the best surgical skill and experience, and further 
that delay may mean the unnecessary and permanent sacrifice of the 
patient ’s sight. 


APPENDIX. 


Aural Disease in Relation to Life Insurance. —As the various aural 
lesions involve risks which insurance companies have frequently to con¬ 
sider, it may be well to discuss briefly the risks which—from the aurist’s 
point of view—these patients would impose upon the companies insuring 
them. 

I personally believe that the attempt to reduce the solution of this 
question to a set of dogmatic, unyielding rules would lead in many cases 
not only to injustice and hardships to the individual, but also to a loss to 
the insurance companies of a considerable amount of legitimate business. 
In other words, I believe that each applicant harboring an aural lesion of 
any form should be examined by a competent and experienced aurist, and 
his application decided in accordance with a careful analysis of all the 
data involved in his particular case. 

Among conditions which should determine absolutely a rejection of 
the applicant may be mentioned the following: 

I. Malignant disease (epithelioma or sarcoma) of any part of the organ 
of hearing. 

II. Advanced tuberculous lesions of the auricle (lupus hypertrophicus) 
as pointing to a constitutional tendency unfavorable to longevity. 

III. Chronic middle-ear suppuration, with evidences of a diffuse sup¬ 
purative invasion of the labyrinth, either present or past. 

The above conditions should permanently disbar the patient as an 
applicant for life insurance. 

In a second category may be placed: 

IV. Chronic middle-ear suppuration with any of the following condi¬ 
tions : 

(a) Polypi springing from promontory, region of oval window, or 
from any part of the inner tympanic wall. 

(b) Polypi attached to the inner margin of the osseous meatus (annulus 
tympanicus) or within the attic, which persistently recur after removal. 

(c) Chronic middle-ear suppuration with recurrent exacerbations ol 
acute mastoid inflammation, any one of which may lead to intracranial 
invasion. 

(d) Evidence of cholesteatoma in any part of the tympanomastoid 
cavity. 

(e) Present facial paralysis or a history of past involvement (paraly¬ 
sis) of the facial nerve, not the result of surgical interference. 

The above should absolutely exclude the applicant until the disease 
has been eliminated by surgical intervention. A complete and permanent 
cure can be determined only by a competent aurist and only after a year 
has elapsed since complete cessation of all symptoms. 

587 


588 


APPENDIX 


In contradistinction to the above, I believe that there are many cases 
in which, in spite of a large perforation allowing a certain amount of 
aural discharge, the character of the lesion is such as to involve little or 
no risk to life. On competent expert advice, such an individual might well 
be accepted at an increased premium rate. 

The various acute suppurative lesions involving either tympanum or 
external ear should during their active period absolutely exclude the 
applicant. They are usually amenable to treatment, and complete recov¬ 
ery usually removes any risk involved in the attack. 

In the effort to elucidate this difficult question, many statistics have 
been collected, a large part of which, while of academic interest, does not 
supply a basis for practical deductions. For example, the copious statis¬ 
tics from the general autopsy records of large hospitals— e.g., Pitt’s analysis 
of Guy’s Hospital Reports, showing one death from aural suppuration to 
158 from other causes, and Gruber’s analysis of the autopsies in the Vienna 
General Hospital, showing one death from aural suppuration to 173 from 
other causes—do not bear very strongly on the risks which these lesions 
impose upon insurance companies. What we need to know is in just 
what percentage of all cases does chronic middle-ear suppuration end 
fatally or shorten the patient’s life; and this is a question at present im¬ 
possible of solution. 

The determination, from the records of an institution specialized for 
the treatment of aural disease, of the proportion of deaths from aural 
suppuration to the total number of aural lesions treated, does not supply 
reliable data; for the more serious cases of aural disease and of intracranial 
lesions resulting therefrom are naturally sent to such an institution, and 
there is no way of correctly computing the large number of individuals 
with chronic middle-ear suppuration who are treated in other institutions, 
by private physicians, or who are content to go without treatment. 

Artificial Aids to Hearing.—Among these may be mentioned Toyn¬ 
bee’s and other artificial drum membranes, paper disks employed as 
substitutes therefor, the various ear-trumpets, Rhodes’s audiphone, the 
acousticon, etc. 

Toynbee’s artificial drum consists of a circular disk of rubber, one side 
of which is provided with a central loop or eyelet, through which is passed 
a thread by which it may be withdrawn or controlled. It is used in cases 
in which a perforation of the drum membrane is supposed to interfere 
with the efficient transmission of sound-waves. The surface to come in 
contact with the remnant of drum membrane may be lightly covered 
with sterile albolene. After it has been applied its position should be 
shifted, the hearing being tested meanwhile to note the effect upon audi¬ 
tion. In some cases functional improvement results; very much oftener 
no gain can be demonstrated. Obviously its use is contra-indicated in 
cases of active suppuration,— i.e., in cases in which the perforation pro¬ 
vides a necessary pathway for the escape of pus or serum. 

A substitute for the above may be improvised by flattening a minute 


APPENDIX 


589 


ball of sterile absorbent cotton, cutting away the edges to give it a circular 
form, and covering the surface to be applied with sterile vaseline or albo- 
lene. This in some cases materially augments the hearing power. More 
often it does not, and it may collect germs and provide favorable condi¬ 
tions for their growth. 

In cases of dry perforations of moderate size, the application of small 
disks of paper, cut to appropriate size and soaked in alcohol, is sometimes 
of value, and is infinitely cleaner than either of the foregoing. 

Rhodes’s audiphone consists essentially of a flexible fan-shaped sheet 
of hard rubber, one edge of which is placed in contact with the upper 
incisor teeth. Sound-waves impinging upon it are transmitted through 
the teeth and cranial bones to the ear. It is a rational effort to utilize 
the increased bone conduction characteristic of tympanic disease, and will 
undoubtedly augment the hearing power in many cases. 

The various ear-trumpets are mechanisms all of which are designed to 
provide a larger and more effective receptacle for sound-waves than is the 
cavity of the concha. When provided with a tube and mouth-piece into 
which the person he is conversing with directly speaks, its effectiveness 
is naturally greatly increased. All of the ear-trumpets and tubes are 
open to the objection, which with many of the hard-of-hearing overbalances 
their value, that they render the individual more or less conspicuous and 
do not enable him to take any part in a general conversation. 

The aurophone, though of undoubted value to many individuals, 
seems without value to others suffering apparently from similar lesions. 
One difficulty with this and similar instruments is that, while the sound 
of the human voice is intensified, so also are the other multitudinous 
(but to the patient unappreciable) sounds which constantly surround 
him,—this resulting in a sort of artificial tinnitus aurium, to which some 
individuals never become accustomed. 

It is regrettable that the application of the various artificial aids to 
hearing have not yet been placed upon any scientific or practically avail¬ 
able basis, enabling the aurist to determine from his aural examination 
just what instrument will best suit the individual patient. Very largely 
it is a matter which can be decided only by the patient’s personal experi¬ 
ments with the different instruments. 

Case Histories.—For the convenience of those wishing to enter upon a 
systematic clinical study of otology, we append below two history forms, 
or charts, which have proved most satisfactory in the author’s practice. 

The shorter of the two (No. 1) was especially designed for bed¬ 
side histories, and enables the physician to record the essential clini¬ 
cal facts in a case of acute tympanic or mastoid disease with a minimum 
expenditure of time and effort. 

No. 2 is used wholly for recording the results of office exami¬ 
nations, and facilitates the taking of adequate histories in cases of 
chronic aural disease. 


590 


APPENDIX 


History Chart No. 1 . (for bedside histories) 
















APPENDIX 


591 


History Chart No. 2. (for office histories) 


Name---Age_ Occupation. 

Date---Address__Referred by 


Symptom for which relief is chiefly sought 

General History 


Diatheses_Heredity 

Aural History 


Physical Examination 



Remarks 


LfT 



Condition of Eustachian tubes. 

RIGHT. 

LEFT. 

REMARKS 



Hearing TetU 

RIGHT 

BEFORE AfTCR 

LEFT 

BEFORE AFTER 

VESTIBULAR TESTS 

Spontaneous nystagmus. Right } . Left ) . 

Welch or Acoumeter 





Puiula tot?.. . —. 

Caloric test. Right. Left .. 

Rotation after nritagmu, „ .. _ .. 

REMARKS. 

Voice or Whiiper 





Lower lone limit 





Upper tone limit 





B. C., fork 





Rinn4 





WEBER REMARKS 

Uiine 

Blood 


Diagnosis_—- Prognosis 

Remarks. 


Treatment. 







































































592 


APPENDIX 


Formulae. —Appended below is a short list of formulae, or prescrip¬ 
tions, which in the author’s experience have proved their value in 
practical otology. 

Alkaline and Antiseptic Solutions for Cleansing the Nasal and Nasopharyn¬ 
geal Spaces. 

1. R Sodii bicarbonat., 

Sodii borat., 

Sodii chlorid., aa gr. x; 

Aquae dest., oz. j. 

Sig.— A non-irritating alkaline spray useful in cases in which all antiseptic drugs, 
even in weak solution, prove irritating. 

2. Sodii bicarbonat., 

Sodii borat., aa gr. xl; 

Glycerini, oz. j; 

Aquae dest., ad oz. iv. 

Sig.—Mildly astringent alkaline spray useful in some cases of nasopharyngeal 
congestion. 

3. R (Dobell’s solution). 

Acid, carbolic., gr. iv; 

Sodii bicarbonat., 

Sodii borat., aa gr. xl; 

Aquae dest., q.s. oz. iv. 

Sig.—Antiseptic spray useful in bacterial infections of nose or nasopharynx. 

4. R Alkalol. 

A proprietary preparation, alkaline, non-irritating, and slightly astringent; may be 
used as nasal spray undiluted. 


Oil Solutions. 


5. 


R 

Menthol, 

gr. iij 




Albolini, 

oz. j. 


Sig.—Nasal spray. 




6. 


R 

Menthol, 

gr. x; 




Albolini, 

oz. j. 


Sig.—Nasal spray. 




7. 


R 

Menthol, 





Camphor, 

aa gr. vj 




Albolini, 

oz. j. 


Sig.—Nasal spray. 


N. B.—The use of an aqueous solution in the nose should be immediately followed 
by an alboline spray, the coating of oil thus supplied being distinctly protective to the 
mucous membrane, particularly if the patient is going immediately out into the open air. 

The use of the weaker or stronger menthol solution depends in part upon whether 
it is intended to allay congestion or mildly to stimulate the mucosa; and also to some 
extent upon individual differences in susceptibility to the local action of the drug. 

The addition of camphor is useful in some cases in relieving turbinal congestion. 


APPENDIX 


593 


Astringent and Antiseptic Solutions for Direct Application to the Pharyn¬ 
geal Mouth of the Eustachian Tube. 

R Argenti nitratis, gr. x; 

Aquae dest., oz. j. 

Sig. Apply locally by means of cotton applicator 

9- R Argenti nitratis, gr. xx; 

Sig.—Apply locally. ^ deS ‘-’ ° Z ' j ' 

10 - R Argenti nitratis, gr. xxx; 

Aquae dest., oz. j. 

Sig.—Apply locally. 

N. B. Nitrate of silver in the above strengths is well borne by the nasopharyngeal 
and tubal mucosa. It is best, however, to begin with the weakest solution (gr. x ad oz. 
j) and gradually increase the strength of the solution. A solution of 30 grains to the 
ounce has in the writer’s experience been as strong as can be advantageously used in 
this region. In using the Yankauer or the ordinary wire applicator for applying nitrate 
of silver solutions throughout the entire length of the canal, a solution of 10 or 20 
grains to the ounce is as strong as should be used. 


11. 

R 

Argyrol, 25 per cent, solution. 

12. 

R 

Argyrol, 50 per cent, solution. 

13. 

R 

Ichthyol, 50 per cent, solution. 


N. B.—As substitutes for silver nitrate the above are very useful. Argyrol is 
strongly antiseptic and at the same time practically non-irritating. For application 
throughout the length of the Eustachian tube, argyrol in 25 per cent, or 50 per cent, 
solution is a safe drug which exerts a distinctly beneficial influence in many cases of 
tubal catarrh. 


Ointments. 

(Used in otological practice chiefly in the treatment of eczematous affections of the 

auditory meatus and auricle.) 

14. R Unguent, zinc, oxid., oz. ss; 

Petrolati, q.s. ad oz. j.—M. 

Sig.—Local application in acute auricular eczema. The parts should be kept con¬ 
stantly coated with the ointment. 

15. R Ichthyoli, dr. j; 

Unguent, zinc, oxid., dr. iij; 

Petrolati, q.s. ad oz. j.-M. 

Sig.—Indicated in acute auricular eczema with denuded surface or considerable 
inflammatory reaction. 

♦ 

16. R Acidi carbolic., gtt. iij; 

Unguent, zinc, oxid., dr. iv; 

Petrolati, q.s. ad oz. j.—M. 

Sig.—Indicated in acute auricular eczema with excessive secretion of pus. 

38 


594 


APPENDIX 


17 R Unguent, hydrarg. oxid. rub., dr. ij; 

Unguent, aquae rosae, q.s. ad oz. j.—M. 

Sig.—Indicated in chronic eczema of meatus or auricle. 


Cleansing Fluid for Irrigating the External Auditory Meatus. 

18. R Acid, carbolic., 1 in 200 solution. 

Sig.—For irrigating meatus preparatory to myringotomy or tympanic operation; 
not suitable for routine use. 

19. R Hydrargyri bichlorid., 1 in 2000 solution. 

Sig.—For cleansing the auditory canal preparatory to myringotomy. Bichloride 
of mercury even in weak solution is, in the author’s opinion, too irritating for routine 
or home use. 

20. R Acid, boric., oz. iv. 

Sig.—Dissolve half a drachm in cup of boiled water. A non-irritating solution which 
is the best irrigating fluid for routine cleansing of the ears. 


Solutions for Instillation into the Ears. 

21. R Sodii bicarbonat., 

Sodii biborat., aa gr. x; 

Aquae, oz. j. 

Sig.—Good solvent of hardened cerumen, when latter cannot otherwise be removed 
without injuring canal. 

22. R Acid, boric., gr. xx; 

Alcohol, 95 per cent., oz. j. 

Sig.—Fill auditory canal and retain 4 to 5 minutes. A cleansing solution which 
promotes healing in purulent otitis media after the acute stage has passed. 

23. R Acid, carbolic., gr. ij; 

Acid, tannic., gr. x; 

Aquae dest., oz. j. 

Sig.—Ten or twenty drops in ear night and morning. Useful in certain cases of 
subacute otitis media, with only moderate discharge. 

24. R Acid, salicylic., gr. x; 

Alcohol, oz. j. 

Sig.—Fill auditory canal night and morning and allow to remain 5 to 10 minutes. 
Almost a local specific against the various forms of aspergilli occasionally lodging in the 
ear. 


Local Anesthesia for Operation of Myringotomy. 

25. R Cocain. hydrochlor., 

Acid, carbolic., aa gr. xlviij; 

Aquae dest., oz. j. 

Sig.—A small round pledget of sterile absorbent cotton is saturated with this fluid 
and the excess shaken off. It is then placed in contact with the drum membrane and 
allowed to remain about two minutes. Drum membrane should then be immediately 
incised. In some cases absolutely no pain is felt; in others some pain is experienced. 


APPENDIX 


595 


robably in all cases the pain is lessened. While stronger solutions of carbolic acid 
have been advised and will more surely induce local anaesthesia, there is distinct danger 
ol permanent injury of the drum membrane by carbolic solutions of greater than 10 
per cent, strength. Even in this strength the solution is advised only in cases in which 
nitrous oxide cannot be given, general anaesthesia, in the writer’s view, being always 
preferable. 


Foe the Relief of Moderate Pain. 

26. R Codeinae, 

Phenacetini, 

Salol, 

M. Divid. in capsul. No. viij. 

Sig.—One capsule t. i. d. 

Certain cases characterized by persistence of moderate ear pain even after incision 
of the drum-head are relieved by two or three doses of the above. 


gr- j; 

aa gr. xx. 


For the Relief of Nasopharyngeal and Tubal Congestion. 

27. R Extract, belladonnae, gr. j; 

Salol, gr. xx. 

M. Divid. in capsul. No. viij. 

Sig.—One capsule q. 4 h. 

Rheumatic or plethoric patients suffering from acute suppurative otitis media often 
exhibit intractable nasopharyngeal congestion. In such cases this formula is often of 
value. 

28. R Tablets (Lincoln’s formula) each to contain 

Extract, belladonnae, gr. y s ; 

Camphor., gr. %; 

Quinin. sulphat., gr. %. 

Sig.—One tablet q. 3 h. Useful in reducing obstinate nasopharyngeal congestion. 

29. R Extract, rhei fluid., 

Sodii bicarbonat., 

Spirit, piper, menth., aa dr. j; 

Aquae dest., q.s. ad oz. iv. 

Sig.—One teaspoonful in wineglass of water t. i. d., a. c. 

This well-known formula is repeated here chiefly on account of the author’s experi¬ 
ence as to its rather wide range of usefulness. For children with acute auricular eczema, 
plethoric adults suffering from furunculosis of the meatus, and rheumatic individuals 
suffering from subacute tympanic disease, there is no question that the administration 
of this mixture is often a positive factor in bringing about recovery. 







INDEX. 


Abducens nerve, origin and position of, 187 
paralysis of, 187 

pathways of infection, from mas¬ 
toid, 188 

Abnormal relaxation of membrana tym- 
pani signs of, 228 

Abscess, Bezold’s, anatomical basis of, 1S7 
nature of, 1S7 
physical signs of, 187 
cerebellar, 375, 502 
extradural (see Extradural abscess) 
of the brain (see Brain, abscess of) 
of the cerebellum (see Cerebellum, 
abscess of) 

perisinous, pathology of, 340 
pathways of pus from, 341 
prognosis and treatment of, 343 
symptoms of, 342 
subperiosteal, 185, 216 
Absolute deafness, bilateral, 92 

unilateral, determination, 92 
Accidental dislocation of stapes during 
myringotomy, 400-402 
during radical operation, 
315, 441 

opening of sigmoid sinus, control of 
hemorrhage from, 424 
Aeoumeter, Politzer ’s, method of using, 80 
normal hearing distance for. 74 
Acquired deaf-mutism, 563 
causes of, 563 

Acute circumscribed external otitis (fu¬ 
runculosis), 107 
treatment of, 111 
disuse external otitis, 116 

treatment of, 116 

inflammatory lesions pf middle ear, 
nomenclature of, 157 • 
purulent inflammation of labyrinth, 
292 

of mastoid cells, 181 
of middle ear, 157 
otitis media in infants, 169 
Adenitis, cervical, associated with inter¬ 
nal jugular phlebitis, 350 
secondary to furunculosis of ex¬ 
ternal auditory canal, 110 
Adenoids, pharyngeal, diagnosis of, 566 

etiological relation of, to tym¬ 
panic disease, 126 
removal of, during acute tym¬ 
panic disease, 568 
treatment of, 567 

Adhesive processes in middle ear, physical 
signs of, 236 


Aditus ad antrum, 34 

landmarks for, 406 
surgical treatment of, during 
mastoidectomy, 419 
After-treatment of mastoidectomy, 426 
radical operation, 451 
Agraphia, motor, 336 
sensory, 335 

Air conduction, hearing by, 73 
Alcohol, aural disorders due to, 130-131 
local use of, in chronic middle-ear 
disease, 208 

Alexander, salvarsan in relation to audi¬ 
tory nerve lesions, 550 
Allport’s self-retaining retractor, 408 
Anaemia as an occasional cause of tinnitus, 
140, 529 

influence of, upon progress of otoscle¬ 
rosis, 250, 257 
of labyrinth, 529 

Anatomical differences between external 
auditory canal of adult and in¬ 
fant at birth, 5 

between external Eustachian tube 
of adult and infant at birth, 30 
Anatomy of external ear, 1 
of inner ear, 260 
of middle ear, 10 

Aneurism of basilar or internal auditory 
artery as occasional cause of objective 
tinnitus aurium, 140 
Annular ligament of stapes, 23 
rupture of, 437 
Annulus tendinosus, 20 
tympanicus, 16 

Anterior pouch of membrana tympani, 25 
tympanic fold, 25 
Antihelix, 2 
fossa of, 2 

Antitragus muscle, 3 
Antrum, position ojf, 32 
surgical guides to, 418 
Aphasia, brief discussion of various types 
of, 331 

citation of interesting cases of, due 
to brain abscess, 372 
in circumscribed leptomeningitis, 
Jansen’s case, 385 
intercortical motor, 335 
motor, 336 

sensorv, due to psychical blindness, 
‘335 

due to word-deafness, 334 
Aphasic centres, chart of, 332 
Apoplectic form of deafness, 527 

597 



598 


INDEX 


Appendages, auricular, 514 
removal of, 521 
Aquaeductus cochleae, 262 

Fallopii (see Facial canal) 
Aquaeductus vestibuli, 266 
Arrested repair following mastoid opera¬ 
tion, treatment of, 429 
Artificial aids to hearing, 570 

drum membrane (Toynbee’s), 570 
Aspergillus flavus, 117 
nidulans, 117 
niger, 117 
Antrium, 11 

Atrophy of drum membrane as a contra¬ 
indication to inflation, 241 
auscultation signs of, during 
inflation, 228 

in chronic hyperplastic oti¬ 
tis media, 237 
physical signs of, 228, 237 

Atropine, 150 
Attic, infection of, 166 
mucous folds in, 26 
spaces, anatomy of, 26 
surgical significance of, 166 
Attolens aurem (musculus auricularis 
superior), 3 

Attrahens aurem (musculus auricularis 
anterior), 3 

Audiphone of Rhodes, 571 
Auditory cortical centre, 273 
hallucinations, 143 

prognostic significance of, 143 
massage, pneumatic, 241 
nerves, basal nuclei and tracts, 273 
cochlear branches of, 272 
vestibular branches of, 272 
ossicles, articulations of, 21 
ligaments of, 21-23 
necrosis of, 213 
removal of, 457 

Aural disease and life insurance, 569 
lesions of caisson workers, 132 

of syphilitic origin, 105, 530, 548 
of tuberculous origin, 532 
pain due to dental lesions, 558 

in acute catarrhal otitis media, 

161 . 

mastoiditis, 183 
perichondritis of auricle, 101 
purulent otitis media, 166 
suppurative labyrinthitis, 
296 

in chronic middle-ear catarrh, 225 
in furunculosis of external audi¬ 
tory meatus, 108 
in herpes zoster auricuke, 106 
polypi, 194, 200, 210 
specula, 48 
syringe, 119 
Auricle, anatomy of, 1 

congenital displacement of, 516 
malformations of, 514 


Auricle, dermatitis of, traumatic, 97 

displacement of, in acute mastoiditis, 

16 

in frunculosis of canal, 110 
eczema of, 98 
epithelioma of, 107 
erysipelas of, 97 
frost-bite of, 98 
function of, 35 
furunculosis of, 110 
haematoma of, 102 
herpetic inflammation of, 106 
lupus of, 104 
muscles of, 2 
operations upon, 518-525 
perichondritis of, 101 
physiology of, 35 
Auricular appendages, 514 

perichondritis secondary to furuncu¬ 
losis of external auditory canal, 110 
Aurophone, 571 

Auscultation sounds during inflation, 65 
tube, 64 

Auscultatory signs of Eustachian catarrh, 
65 

constriction, 65 

of fluid within tympanic cavity, 65 
of perforation of drum mem¬ 
brane, 65 

of relaxed drum membrane, 65, 
228 

Author’s adjustable curette for removing 
foreign bodies from meatus, 121 
labyrinthine curette, 472 
scheme for memorizing position of 
semicircular canals, 285 
tuning-forks, 88 
tympanic rongeur, 446 

Babinski, pithiatism, 543 
Bacteria associated with acute middle-ear 
inflammation, 159 

Bacteriaemia in infective sigmoid sinus 
thrombosis, 348 

in lesions not of otitic origin, 349 
Bacteriology of brain abscess, 359 
Ballance, digital exploration of brain for 
suspected abscess, 493 
metal flap in radical operation, 450 
Bandage for mastoid dressing, 427 
Banti’s case of motor aphasia, 373 
Barany, caloric reactions, 280 

cerebellar localization, theory of, 394 
changes in pointing accuracy in cere- 
, bellar and labyrinthine disease, 379 
laws governing interrelation of ves¬ 
tibular nystagmus, vertigo, and 
ataxia, 288-289 

rules for inducing different forms of 
nystagmus following rotation, 291 
Barany’s noise apparatus, 93 
Barr, statistics bearing upon usual sites 
of otitic brain abscess, 358 


INDEX 


Bell, Graham, parental consanguinity in 
relation to spread of deaf-mutism, 
563 

Benario, J., cranial nerve lesions follow¬ 
ing administration of mercury, 551 
statistics relating to auditory nerve 
lesions following salvarsan, 549 
Berens, T. Passmore, rongeur method of 
opening mastoid, 321 
Bezold, character of deafness in acute 
catarrhal otitis media, 162 
etiology of otomycosis, 117 
explanation of increased bone con¬ 
duction in tympanic disease, 77 
influence of alcoholism upon auditory 
function, 131 

nomenclature of acute tympanic 
lesions, 157 

osteotympanic versus molecular the¬ 
ory of sound transmission, 40 
results following surgical opening of 
brain abscess, 490 
Bezold’s abscess, 187 

anatomical basis of, 187 
nature of, 187 
physical signs of, 187 
Bichloride of mercury, injurious effect of, 
upon tympanic structures, 175 
Bing’s test, 91 

Blake, C. J., plastic modification of mas¬ 
toid operation, 430 
Blood-clot operation, 430 
Blood-count in infective sinus thrombosis 
(Crockett), 347 

Blood-cultures, diagnostic value of, 349 
Blood-vessels of labyrinth, 273 
Boils in external auditory meatus (see 
Furunculosis) 

Bondy’s operation for chronic middle-ear 
suppuration, 457 
Bone conduction, hearing by, 73 
Boric acid in treatment of chronic middle- 
ear suppuration, 211, 214 
Bougies, Eustachian, 230 
medicated, 239 
method of using, 231 
use of, in otitis media hyper- 
plastica chronica, 238 
use of, in otitis media hyper- 
trophica chronica, 230 
Bourgeois, war deafness, 538 
Brain abscess, 357 

aphasia in, 371 
bacteriology of, 359 
clinical stages of, 363 
drainage of, 499 
etiology of, 357 
eye-ground changes in, 366 
focal symptoms of, 368 
general symptoms of, 362 
influence of cerebral hernia upon 
prognosis in, 491 
mental disturbances in, 330, 368 


599 

Brain abscess, modes of infection through 
tegmen tympani, 362 

muscular spasms and paralysis 
in, 369 
onset of, 363 
pathology of, 361 
postoperative treatment of, 499 
pupillary changes in, 371 
statistics as to location of, 358 
surgical treatment of, 490 
symptoms of, 362 
technic of exploring temporo- 
sphenoidal lobe, 495 
temperature and pulse changes 
in, 364, 365 
terminal stage of, 374 
pathologic variations in accord¬ 
ance with character of invad¬ 
ing germ, 362 

Brain, intolerance of, to certain forms of 
manipulation, 492 
surgical exploration of, 495 
tolerance of, to rational surgery, 498 
Broca’s convolution, 333, 336 
Bruhl’s plastic (flap) operation, 451 
Bryant, W. S., method of opening the 
mastoid by the digastric route, 320 
tuberculosis of the middle ear. 536 
Bulb of the jugular vein, infection of, 171 

t 

Caisson workers, aural disorders of, 132 
Calcareous degeneration of the drum 
membrane, 227 
Caloric test (Barany), 280, 281 

method of applying, 300 
use of, in latent suppurative 
labyrinthitis, 301 
use of, in suppurative labyrin¬ 
thitis, acute stage, 296 
Canalis reuniens, 266, 270 
Cardiac lesions as an occasional cause of 
objective tinnitus aurium, 139 
Cardinal signs of a retracted drum mem¬ 
brane, 147 

Carotid artery, possible injury to, during 
curettage of the Eustachian tube, 
440 

canal, relation of, to tvmpanic floor, 15 
Catarrh, tubal, 145, 151, i53, 209, 221 
Catheter inflation, danger of rupture in 
atrophy of the drum mem¬ 
brane, 237 

in acute tvmpanic disease, 178, 
179 

in catarrh of the Eustachian tube 
222 

in chronic middle-ear catarrh, 
230, 237, 240, 241 
surgical emphysema resulting 
from, 69 
technic of, 65 

value of, as compared with 
politzerization, 151 


600 


INDEX 


Causes of acute tympanic disease, 126 
Cavernous sinus, thrombosis of, 348 
Cells of Retzius, 268 
Cerebellar abscess, 375 

Barany’s symptom of, 379 
diadokokinesis in, 377 
differential diagnosis of, from 
acute labyrinthitis, 
380 

from temporal lobe ab¬ 
scess, 379 

direction and depth of explora¬ 
tory punctures, 502 
disturbance of equilibrium in, 
^ 378 

focal symptoms of, 376 
general symptoms of, 375 
respiratory paralysis in, 379 
surgical treatment of, 502 
terminal stage of, 379 
unilateral incoordination ataxia 
in, 377 

ataxia (static), 378 
nystagmus, 376 
localization, theory of, 394 
Cerebellum, cortical centres of, 394 
Cerebro-spinal fluid, in health and disease, 
390 

Cerumen in external auditory canal, re¬ 
moval of, 123 
Ceruminous glands, 10 
Cervical adenitis (associated with furuncu¬ 
losis of auditory meatus), 110 
(associated with internal jugular 
phlebitis), 350 

Chlorosis, influence of, upon progress of 
otosclerosis, 257 

Cholesteatoma, diagnosis of, 215 

effect upon contiguous bone, 196 
etiological relation of, to intracranial 
disease, 196 

to suppurative labyrinthitis, 
293 

influence of, upon character of aural 
discharge, 198 
pathology of, 195 
spontaneous elimination of, 197 
treatment of, 215 

Chorda tympani nerve, course of, within 
tympanum, 28 
injury to, during myringot¬ 
omy, 402 

Chronic, hyperplastic otitis media (see 
Otitis media hyperplastica chron¬ 
ica) 

hypertrophic otitis media (see Otitis 
media hypertrophica chronica) 
middle-ear suppuration (see Otitis 
media purulenta chronica) 
tubal catarrh, symptoms and physical 
signs of, 219 
treatment of, 222 
Claudius’s cells, 271 


Cocaine, use of, 151 
Cochlea, anatomy of, 260 
Cochlea, aqueduct of, 262 
function of, 274 
membranous structures of, 269 
spiral ligament of, 270 
Cochlear nerve, 272 
Cochleo-palpebral test (Gault), 545 
Cold, application of, to mastoid, 189 
Comparative frequency of temporal lobe 
and cerebellar abscess, statistics, 358 
Complications of acute purulent otitis 
media, 170 
Concha, 2 

function of, 36 

abnormal development of, 516 
Concussion deafness, 538 
Congenital deaf-mutism, 561 
treatment of, 565 
. malformations of ear, 514 

surgical correction of, 519 
Consanguinity, parental, in relation to 
deaf-mutism, 562 

Consonants, fundamental tones of, 81 
Conversational speech, method of testing 
by, 82 

normal hearing distance, for, 75 
sound values of various compo¬ 
nents of, 81 

Corrosive sublimate, injurious effects of, 
upon tympanic structures, 175 
Corti, organ of, 270 
rods of, 270 
tunnel of, 271 

Cortical centre for sound memories, 332, 
333 

hearing centre, 273 
memory centre for motor writing 
efforts, 332 

for motor speech efforts, 333 
for tactile impressions, 333 
for visual impressions, 333 
C ranial nerve lesions, salvarsan in relation 
to, 538 

Crista vestibuli, 263 
Cristae acusticae, 267 

Crockett, E. A., blood count in infective 
sinus thrombosis, 347 
optic neuritis in infective thrombosis, 
347 

tuberculosis of the middle ear and 
mastoid, 536 
Cupola, 268 

Curvature of membrana tympani, influ¬ 
ence of, upon sound conduction, 36 
Cushing, Harvey: 8th nerve tumors, 
chronology of symptoms 
of, 578 

interval between initial and 
later symptoms, 584 
statistics of, 572 
subcapsular versus capsular 
removal, 585 


INDEX 


601 


Dakin’s fluid, use of in aural disease, 453 
Dana, C. L., auditory nerve tracts, 273 
neurasthenia as a cause of tinnitus 
aurium, 142 
Deaf-mutism, 561 

causes of acquired form, 563 
etiology of congenital form, 561 
hereditary transmission of, 561 
pathology of, 564 
pithiatic, 543 

relation of parental consanguinity to, 
562 

treatment of, 565 

Deafness, absolute, determination of, 92 
apoplectic form of, 527 
chronic, treatment of, 229, 238, 255 
due to alcoholism, 131 
due to concussion, 541 
hysterical, 543 

in diffuse suppurative labyrinthitis, 
296 

in Meniere’s disease, 527 
leucaemic, 528 
pithiatic, 543 

resulting from parotitis, 128 
simulated, tests for, 93 
surgical measures for the relief of, 258 
Dean, L. W., audiometer, 87 

congenital atresia of auditory canals, 
518 

sensory aphasia in temporosphenoidal 
abscess, 372 

treatment of brain abscesses present¬ 
ing dural fistuke, 491, 495 
Deiters’s cells, 271 
nucleus, 273 

Dench, E. B., inflating apparatus, 63 

protrusion of jugular bulb through 
necrotic defect in tvmpanic floor, 
138 

Denker, non-syphilitic origin of otoscle¬ 
rosis, 244 

Dental lesions causing aural symptoms, 
558 

Dermatitis of auricle, 97 
Development of bony meatus, 4 
Diadokokinesis (Babinsky), 377 
Diagnostic tube, 64 

auscultatory signs obtained 
through, 65 

Diffuse external otitis, acute, 116 
purulent leptomeningitis, 383 
suppurative labyrinthitis, acute stage, 
294 

latent stage, 299 

Dilatation of Eustachian tube, 230-233 
Diphtheria, character and frequency of 
aural complications in, 127 
Diploic mastoid, 32 
Diseases of auricle, 97 

of brain and meninges, 337 
of Eustachian canal, 145, 219 
of external auditory meatus, 107 


Deafness of labyrinth, 278 
of mastoid, 181 
of tympanum, 145 

Disturbance of hearing due to ossicular 
fixation in chronic middle-ear 
catarrh, 224, 235 
in acute myringitis, 156 
in otosclerosis, 251 
in tympanic disease, 162 
resulting from chronic middle- 
ear suppuration, 199 

Disturbances of equilibrium due to vesti- 
ular irritation, 287, 295 
due to vestibular paralysis, 303- 
309 

in cerebellar abscess, 378, 379 
Drum membrane (see Membrana tym- 
pani) 

appearance of, in acute tubal 
catarrh, 147, 148 
in otosclerosis, 253 

in tubotvmpanic congestion, 
149 

Ductus cochlearis (scala media), 270 
Duel, A. B., blood cultures in suppurative 
lesions of ear, 349 

electrolysis in treatment of strictures 
of the Eustachian canal, 233 
Duel’s operation for replacement of pro¬ 
jecting ears, 523 

Dura mater, structural changes in region 
of venous sinuses, 340 

Ear, anatomy of, 1-28 
asymmetry of, 514 
blood-vessels of, 26 
functional examination of, 73-96 
malformation of, 514-525 
nerves of, 27 

physical examination of, 41-69 
syphilis of, 305, 530, 548 
tuberculous affections of, 532-537 
Earache (see Aural pain) 
causes of, 133-134 
in acute catarrhal otitis media, 161 
in chronic catarrhal otitis media, 133 
in purulent otitis media, 166 
reflexly induced by non-aural lesions, 
134 

Eburnation of parts of temporal bone in 
chronic middle-ear suppuration, 194 
Eczema of auricle, acute, 98 
treatment of, 99 
chronic, 100 
treatment of, 100 

Ehrlich’s theory of causation of cranial 
nerve lesions^ following salvarsan, 549 
Electrolysis in treatment of Eustachian 
strictures (Duel), 233 
Embolism, labyrinthine, in caisson work¬ 
ers’ disease, 132 

Emphysema, local, following catheter in¬ 
flation, 69 


602 


INDEX 


Emphysema, prognosis of, 69 
treatment of, 69 
Encephaloscope, Whiting’s, 499 
Endolymph, 260 

Epidural abscess (see Extradural abscess) 
Epithelioma of auricle, 107 
treatment of, 107 
Epitympanic space, 10 
Erysipelas of auricle, 97 
treatment of, 97 

Eustachian bougies, method of using, 230 
varieties of, 230 
canal, acute lesions of, 145-155 
anatomy of, 28-31 
catarrh of (see Tubal catarrh) 
catheterization of, 63 
chronic lesions of, 219 
differences in infant and adult, 
30 

muscles of, 31 

pharyngeal orifice of, 29, 31 
physiology of, 30 
structural narrowing of, 222 
tympanic orifice of, 29, 31 
Yankauer’s method of curetting, 
209 

catheter, correct type of, 63 
Ewald’s experiments upon semicircular 
canals of pigeons, 278 
theory of vestibular control of muscle 
tonus, 276 

Examination of auricle and external audi¬ 
tory canal, 43 

of drum membrane and middle ear, 53 
of Eustachian tubes, 60 
of nose, nasopharynx, and throat, 69 
of patient^ 41 

Exostoses of osseous meatus, 125 
External auditory canal, acute diffuse in¬ 
flammation of, 116 
anatomy of, 4 
bony outgrowths from, 125 
comparison of infantile and 
adult types, 7 
development of, 4 
eczema of, 100 
furunculosis of, 107 
lining membrane of, 10 
membranocartilaginous por¬ 
tion of, 4 
mycosis of, 117 
operations for removal of 
foreign body from, 122 
osseous portion of, 8 
removal of cerumen from, 
123 

removal of foreign bodies 
from, 119 

variation in length and direc¬ 
tion of, 9 

otitis, acute circumscribed (see Fu¬ 
runculosis of meatus) 
diffuse, 115 


Extradural abscess, etiology of, 338 
prognosis of, 339 
symptoms and physical signs of, 
338 

treatment of, 340 

Eye-ground changes in intracranial lesions 
of otitic origin, 366 

Facial canal, 11; course of, 408 

nerve, branch of, to stapedius muscle, 
28 

possible injury to, in radical 
operation, 442 

relation of, to aditus ad antrum, 
419 

to ampullae of horizontal and 
anterior vertical semicir¬ 
cular canals, 463 
paralysis, brief discussion of, 442 
otitic, causes of, 508 
prognosis of, 508 
postoperative, faciohypoglossal 
neurorrhaphy for, 511 
prognosis and treatment of, 
510 

symptoms and signs of, 509 
Faciohypoglossal anastomosis, 511 
Fallopian aqueduct (facial canal), 408, 419, 
442, 463 

Fenestra ovalis, 11 
rotunda, 11 
Fissura intertragica, 2 
Fissures of Santorini, 4 
Fistula test, diagnostic value of, 299 
method of applying, 298 
Folds of drum membrane, 25 
anterior, 25 
posterior, 25 

Fordyce, John A., method of administering 
salvarsan yielding best results, 553 
relation of salvarsan to disease of 
cranial nerves, 552 

Forehead mirror, correct type for aural 
work, 45 

method of using, 52 

Foreign bodies in external auditory canal, 
removal of, 119 
surgical removal of, 

122 

Formulae, 574 
Fossa cochlearis, 262 
incudis, 22 

Fovea elliptica (recessus ellipticus), 263 
hemispherica (recessus hemispheri- 
cus), 267 

Frazer, J. S., deafmutism, 565 
otosclerosis, 247 
Frost-bite, auricular, 98 
treatment of, 98 

Function of tympanic muscles, Mach’s 
theory of, 39 

Functional examination of cochlear ap¬ 
paratus (hearing tests), 73 


INDEX 


603 


Fungi in external auditory meatus, 117 
Furunculosis of external auditory meatus. 

107 

deformities resulting 
from, 110 

differential diagnosis of, 

110 

etiology of, 107 
prognosis of, 111 
stages of, 112 

Furunculosis of external auditory meatus, 

symptoms and physical 
signs of, 108 
treatment of, 111 
vaccine therapy in, 115 

Galton whistle, use of, 86 
Galvanic test of vestibular irritability, 303 
Ganglion, spiral, 269, 272 
Gault’s cochleo-palpebral test, 545 
Gauze wicks, use of, in acute purulent 
otitis media, 177, 178 
in brain abscess, 500, 501 
Gelle’s test, 91 

Geniculate ganglion, inflammation of, 106 
Glossopharyngeal nerve, 27 
Goldstein, M. A., primary tuberculosis of 
middle ear, 536 

Goldstein’s operation for projecting uari- 
cles, 520 

Gout and rheumatism as a predisposing 
cause of auricular eczema, 99 
as a predisposing cause of furun¬ 
culosis of canal, 108 
as a predisposing cause of tym¬ 
panic disease, 41 

Gowers, significance of tinnitus aurium of 
cerebral type, 143 

Gradenigo, circumscribed leptomeningitis 
with recovery following operation, 386 
Gradenigo’s symptom-complex, 188 
Gram-negative anaerobic bacilli, relation 
of, to pathology of brain abscess (New- 
mann), 361 

Grant, Dundas, nervous exhaustion as a 
cause of tinnitus aurium, 142 
neurasthenia as an occasional 
cause of hyperacusis, 142 
Gray, A. A., biologic aspects of oto¬ 
sclerosis, 246 

theory as to pathogenesis of oto¬ 
sclerosis, 249, 250 
theory of tone perception, 276 
Grippe as a cause of aural disease, 128 
Gruening, case of multiple metastatic 
abscess secondary to infective sinus 
thrombosis, 354 

corroborative value of blood exami¬ 
nations in diagnosis of infective 
sinus thrombosis, 348 
headache and mental lethargy in in¬ 
fective sigmoid sinus thrombosis, 347 
Grunert, etiology of brain abscess, 358 


Haematoma auris (orthaematoma), 102 
Hair-cells of Corti’s organ, 271 

of cristae acusticae ard maculae acus- 
ticae, 267 

Hallucinations, auditory, 143 
Hammer (malleus), 16 
Handle of malleus, 18 
Hartmann s differential test in otosclero¬ 
sis, 253 

tuning-forks, 83 

Hasslauer, bacteriology of brain abscess, 
359, 360 

Headache in cerebellar abscess, 375, 380 
in otitic leptomeningitis, 383 
in sigmoid sinus thrombosis, signifi¬ 
cance of, 347 

in temporosphenoidal abscess, 363 
of reflex origin, 558 

Head-mirror suitable for aural work, 45 
Head-rest for mastoid surgery', 411 
Hearing by bone conduction, 73 

conduction, Bezold’s expla¬ 
nation of increase of, in 
ty'mpanic disease, 77 
changes in, 77 

diagnostic significance of in¬ 
crease in, 78 

normal ratio of, to air con¬ 
duction, 73 

significance of diminution of, 
79 

Hearing centre in cerebral cortex, 273 

power, influence of radical operation 
upon, 455 
tests, 73 

Heat, application of, to ear, 173 
Heath’s operation for chronic middle-ear 
suppuration, 455 

Heimann, statistics bearing upon usual 
location of brain abscess, 358 
Heine, safety limits in exploratory punc¬ 
tures of brain, 499 
treatment of brain abscess, 491 
Helicis major, 3 
minor, 3 

Helicotrema, 262 
Helix, 1 

abnormalities of, 514 
fossa of, 1 

Helmholtz, greater resonance of curved 
membranes as compared with flat, 
37 

on relative maximum movements of 
different ossicles, 38 

Helmholtz’s theory of tone analysis, 274 
Hemorrhage due to accidental opening of 
sigmoid sinus during mastoid opera¬ 
tion, 424 

in exploratory operations upon sig¬ 
moid sinus, 483 
into labyrinth, 526 

Henle’s spine (suprameatal spine), 406 
Hensen’s cells, 271 


604 


INDEX 


Heredity in relation to congenital deaf- 
mutism, 561, 563 
to otosclerosis, 245 
to primary middle-ear tubercu¬ 
losis, 532 

Hernia cerebri, prevention of, 491 

prognostic significance of, in 
brain abscess, 491 

Herpes zoster auricula?, Hunt’s disease, 106 
Hinsberg, comparative mortality in cases 
of suppurative labyrinthitis treated 
with and without surgical interven¬ 
tion, 315 

Hinsberg, percentage of cases of middle- 
ear suppuration developing labyrin¬ 
thitis, 293 

stapedial injuries as a cause of sup¬ 
purative labyrinthitis, 292 
Hinsberg’s operation for suppurative laby¬ 
rinthitis, 466 

Horsley, Sir Victor, orientation of points 
of space, 305 

Hudson-Makuen, treatment of deaf-mut- 
ism, 565 

Hunt, J. Ramsey, inflammation of genic¬ 
ulate ganglion, 106 

Hyperacusis as an occasional phenomenon 
of neurasthenia, 142 
Hvpersemia of the labyrinth, 314 
Hvpoglossal nerve, surgical exposure of, 
511 

Hypotympanic space, 10 

surigcal treatment of, in radical 
operation, 439 

Ice-bag, application of, to mastoid, 189 
Impacted cerumen in external auditory 
canal, 124 

Incisura intertragica, 2 
Incoordination ataxia in cerebellar dis¬ 
ease, 377 

Incus, anatomy of, 18 

articulation of, with malleus, 22 
with stapes, 23 
long arm of, 23 
short process of, 22 

Indications for incising drum membrane, 
399 

for opening mastoid, 191 
for performing the radical mastoid 
operation, 216 

for resection or ligation of internal 
jugular vein, 478 

for surgical drainage of labyrinth, 463 
for surgical exploration of sigmoid 
sinus, 355 

Infant skull, position of temporal bone in 6 
Infant’s Eustachian tube, 30 
external auditory meatus, 7 
temporal bone, 6 

Infants and young children, acute mas¬ 
toiditis (i.e., antritis) in, 
187-188 


Infants and young children, acute purulent 
otitis mediain, 169-171 
tubal catarrh in, 153-155 
Infectious diseases, relation of, to acute 
tympanic disease, 127, 129 
Infective sigmoid sinus thrombosis, 343 

aspiration movements 
of sinus wall, signifi¬ 
cance of, in, 352 
bacterimmia in, 348 
etiology of, 344 
indications for opening 
sinus in, 355 
sinus thrombosis, liga¬ 
tion versus resection 
of jugular vein in, 478 
macroscopic changes in 
sinus wall in, 350 
pathology of, 344 
prognosis of, 354 
rationale of treatment 
of, 356 

resection versus ligation 
of jugular vein in, 477 
surgical treatment of, 
477 

symptoms of, 345 

Inflammation of geniculate ganglion, 106 
Inflation of ears by catheter, 63 
Politzer’s method of, 61 
Valsalva’s method of, 60 
Influenza as a cause of acute tympanic 
disease, 128 

Initial incision for exposure of cerebellum, 
504 

of jugular vein, 486 
of temporosphenoid lobe, 493 
for radical operation, 433 
for simple mastoid operation, 413 
Inner tympanic wall, landmarks of, 11 
Insects in external auditory meatus, re¬ 
moval of, 120 

Internal auditory meatus, injury to, during 
labyrinthine operation, 474 
jugular vein, infection of, 350 
ligation of, 488 
resection of, 485 
resection versus simple liga¬ 
tion of, 477 

Intracranial complications of tympanic 
disease, 337 

disease, symptoms of, 322 
lesions of otitic origin, pathways of 
infection from tympanum or mas¬ 
toid, 337 

Intratympanic muscles, 23 

operations for improvement of hear¬ 
ing, 258 

Isthmus of Eustachian tube, 28 
of external auditory meatus, 8 

Jackson, Hughlings, muscular spasms in 
lesions of cerebral cortex, 326 


INDEX 


605 


Jacobson’s nerve, 27 

Jansen, circumscribed purulent leptomen¬ 
ingitis with recovery after opera¬ 
tion, 385 

mortality following surgical injury to 
labyrinthine capsule, 317 
surgical injuries as a cause of suppu¬ 
rative labyrinthitis, 292 
Jansen’s chisels, 408 

operation for suppurative labyrinthi¬ 
tis, 465 

statistics bearing upon etiology 7 of 
brain abscess, 358 

Jugular bulb, infection of, without inter¬ 
mediate mastoid disease, 171 
possible injury to, during my¬ 
ringotomy, 400 
relation to tympanic floor, 15 
vein, infection o£ 350 
ligation of, 477, 488 
resection of, 477, 485 

Keith, Sir Arthur, theory of tone percep¬ 
tion, 276 

Kerley, C. G., frequent absence of pain in 
young children suffering from o. m. p. a., 
169 

Kerrison, abducens nerve paralysis, case 
report of, 188 

cerebellar abscess, case report of, 378 
operation for closing post-auricular 
opening, 462 

otitic meningitis, case report of, 388 
scheme for remembering semicircular 
canal planes, 286 

vertigo of vestibular paralysis, 303 
Knapp, Arnold, circumscribed leptomen¬ 
ingitis, 386 

Korner, etiology of otosclerosis, 244, 245 
frequency of fistulae in otitic brain 
abscess, 492 

influence of pregnancy upon the ad¬ 
vance of otosclerosis, 254 
necessity of conservatism in advising 
the radical operation, 216 
statistics bearing upon usual loca¬ 
tions of brain abscess, 358 
Korner’s plastic (flap) operation, 449 

Labium tympanicus, 269 
vestibulare, 269 
Labyrinth, anaemia of, 529 
anatomy of, 260 
blood-vessels of, 273 
function of, 274 
hyperaemia of, 314 
indications for operating upon, 463 
leukaemia of, 528 
membranous structures of, 265 
nerves of, 272, 273 
non-suppurative disorders of, 526 
operations upon, 463 
osseous portion of, 260 


Labyrinth, physiology of, 274 

structural abnormalities of, in deaf- 
mutes, 564 

changes resulting from otosclero¬ 
sis, 245 

suppurative lesions of, 278 
surgical guides to the vestibule of, 464 
syphilis of, 530 

technic of openingthe vestibule of, 470 
tuberculosis of, 532 

Labyrinthine fistula, prognostic signifi¬ 
cance of, 298 
symptoms of, 298 

infection, frequency of, in suppurative 
otitis media, 293 
pathways of, 292 
vestibule, surgical guides to, 464 
Labyrinthitis, circumscribed suppurative, 
differential diagnosis of, 
from other labyrinthine 
lesions, 313 
symptoms of, 310 
treatment of, 317 
usual site of, 309 

diffuse serous, differential diagnosis of, 
from other labyrinthine lesions, 
313 

prognosis of, 311 
symptoms of, 311 
treatment of, 318 

diffuse suppurative, acute stage of, 
294 

caloric test in acute stage of, 
296 

caloric test in latent stage 
of, 300 

cholesteatoma as a cause of, 
293 

complications of, 309 
differential diagnosis from 
cerebellar ab¬ 
scess, 380 
from other laby¬ 
rinthine le¬ 
sions, 313 

disturbance of cochlear func¬ 
tion in, 296 

estimated mortality in cases 
not operated upon, 314 
etiology of, 292 
frequency of (Hinsberg, von 
Stein), 293 

high mortality in cases re¬ 
sulting from stapedial in¬ 
juries, 315 
latent stage of, 299 
stapedial injuries as a cause 
of, 292 

surgical operations for relief 
of, 463 

symptoms of, 294 
treatment of, 314 
value of fistula test in, 298 


606 


INDEX 


Lake, Richard, leukaemia of labyrinth, 529 
tonsillectomy in cases of otosclero¬ 
sis, 257 

vertigo in otosclerosis, 252 
Lake’s operation for relief of vertigo, 475 
Lamina spiralis, 269 
Landmarks of inner tympanic wall, 11 
of mastoid cortex, 406 
of normal drum membrane, 53 
Langenbeck’s periosteal elevator, 407 
Lateral sinus, dural covering of, 340 
suppurative disease of, 343 
ventricle, puncture of, 505 
Leiter’s coil, application of, to mastoid, 
189 

Leptomeningitis, circumscribed, symp¬ 
toms of, 385 
treatment of, 392 

diffuse purulent, pupillary and eye- 
ground changes in, 384 
surgical treatment of, 506- 
507 

symptoms of, 383-385 
treatment of, 389-393 
Leukaemic deafness, 528 
Levator palati muscle, 31 
Libman, value of blood cultures in sig¬ 
moid sinus thrombosis, 348 
Life insurance, relation of aural disease to, 
569 

Ligamentum spirale cochleae, 270 
Ligation of jugular vein in sigmoid sinus 
thrombosis, 488 

Light, arrangement of, for aural work, 49 
reflex, 55 

Lining membrane of Eustachian canal, 29 
of tympanum, 24 
Lobule of ear, 1 
Lombard’s test, 545 
Lop ear (projecting ear), 516 

plastic operations for 
correction of, 520 

Love, J. K., etiology of deaf-mutism, 562, 
564 

Lucae, circumscribed leptomeningitis with 
recovery following operation, 386 
Lumbar puncture, 385, 387, 393 
Lupus hypertrophicus, 105 
of auricle, 104-105 

McCaw, J. F., primary tuberculosis of 
middle ear, 536 

Macewen, pathology of brain abscess, 362 
pupillary changes in brain abscess, 371 
McKernon, J. F., infection of jugular bulb 
without mastoid involvement, 171 
sensory aphasia in temporosphenoidal 
abscess, 372 

treatment of brain abscess, 500 
Mach’s theory of function of tympanic 
muscles, 39 

Macrotia, common types of, 514 
surgical correction of, 520 


Macula acustica of saccule, 267 
of utricle, 266 
Maculae cribrosae, 264 
Malformations of ear, congenital, 514 
correction of, 516 
Malignant disease of auricle, 107 
Malingering, simulated deafness, tests 
for, 93 

Malleus, anatomy of, 16 
articulation of, 21 
ligaments of, 22 

Manubrium mallei (hammer handle), 18 
maximum excursions of, 38 
Marginal perforations of membrana tym- 
pani, pathological significance of, 193, 
202, 211 

Massage (pneumatic) of drum membrane 
and ossicles, 241 

Mastoid perforation in chronic middle- 
ear suppuration, significance of (My- 
gind), 216 

Mastoid process, absence of, in foetus, 182 
anatomy of, 31 

changes in, as a result of 
chronic middle-ear suppura¬ 
tion, 194 

indications for opening, 190 
operations upon, 413 
structural variations of, 32 
suppurative inflammation of, 181 
perforation of cortex of, 182 
185, 187, 216 

surgical landmarks of, 406 
Mastoidectomy, accidental opening of 
sigmoid sinus in, 424-425 
after-treatment of wound, 427-430 
arrested tissue repair following, treat¬ 
ment of, 429 

element of time ( i.e ., operative speed) 
in, 425 

exposure of normal dura in, 424 
instruments required for, 410 
mastoid operation (Schwartze’s op¬ 
eration), 409 
preparation for, 409 
surgical treatment of the aditus in, 
420 

sutures and wound dressing in, 425 
treatment of mastoid tip in, 417 
of zygomatic cells in, 421 
Mastoiditis, acute suppurative, clinical 
variations corresponding 
to structural variations of 
different temporal bones, 
182 

etiology of, 181 
indication for opening mas¬ 
toid in, 190 

in infants and young chil¬ 
dren, 187 

non-surgical treatment of, 

188 

pathology of, 181 


INDEX 


607 


Mastoiditis, physical signs of, 184 
prognosis of, 188 
surgical treatment of, 409 
symptoms of, 183 
temperature range in, 183 
Measles, character of aural lesions caused 
by, 128 

Meatus, external (see External auditory 
canal) 

Mechanism for control of normal tympanic 
tension, 39 

Medicated bougies, 239 
Medicinal formulae, 568 
Membrana basilaris, 269 

flaccida (see Shrapnell’s membrane) 
spiralis cochleae, 270 
tectoria, anatomy of, 270 
function of, 275 
tensa, anatomy of, 19 
tympani, adhesion of, to tympanic 
wall or structures, 238 
anatomy of, 16, 19 
atrophy of, 237 
calcareous thickening of, 227 
cardinal signs of retraction of, 
147 

central perforations of, 201 
displacement of, 57 
incision of (see Myringotomy) 
landmarks of, 53 
layers of, 19 

marginal perforations of, 203 
objective examination of, 50 
physiology of, 36 
pouches or pockets of, 24 
quadrants of, 55 
removal of, with malleus and 
incus for relief of deafness, 259 
spontaneous rupture of, in otitis 
media catarrhalis acuta, 
161 

in otitis media puru- 
lenta acuta, 167 
structural changes in, 57 
traumatic injuries of, 159 
Membrane of Reissner, 270 
Membrano-cartilasjnous portion of exter¬ 
nal auditory meatus, 4 
of Eustachian tube, 29 
Membranous compartments of tympanic 

vault, 26 

surgical significance of, 
166 

vestibule, obliteration of, for relief of 
vertigo (Lake), 475 
M6neire’s disease, etiology of, 526 

prognosis and treatment of, 527 
symptoms of, 527 

Meningismus, 389 . QOO qo1 

Meningitis, cerebro-spinal fluid in, oyu-dJi 
otitic (see Leptomeningitis) 
serous, surgical treatment of, 504 
symptoms of, 387 


Mental disturbances in brain lesions of 
otitic origin, 330 

Metastatic brain abscess of otitic origin 
(Rae), 353 
Microtia, 516 
Middle ear, 9 

anterior wall of, 13 
blood-vessels of, 26 
floor of, 14 

folds of mucous membrane in, 25 
inflammatory diseases of (see 
Otitis media) 
lining membrane of, 24 
membranous compartments of 
attic, 26 

muscles of, 23, 39 

nerve supply of, 27 

non-suppurative lesions of, 219 

posterior wall of, 14 

roof of, 12 

subdivisions of, 11 

syphilis of, 548 

tuberculosis of, 532 

Milligan, Wm., primary tuberculosis of 
ear, 536 

surgical relief of vertigo, 476 
Mirror, forehead, types of, 45 
use of, 52 
Modiolus, 260 

absence of, in deaf-mutism, 564 
central canal of, 262 
injury to, during labyrinthine opera¬ 
tion, 474 

Mosetig-Moorhof operation, 459 
Motor aphasia, 336 

Banti’s case of, 373 

Mucous membrane of Eustachain tube, 29 
of tympanum, 24 

Mumps, deafness resulting from, 128 
Muscles, intratympanic, 23 
of auricle, 2 
of Eustachian canal, 31 
Muscular spasms (unilateral), interpreta¬ 
tion of, in otitic brain disease, 326, 369 
Mygind, heredity in relation to spread of 
deaf-mutism, 561 
Myringitis, acute, 156 

diagnosis of , 156 
treatment of, 156 

Myringotomy, indications for, 399 

in otitis'media catarrhalis acuta, 174 
in otitis media purulenta acuta, 179 
operative dangers of, 400 
surgical mishaps resulting from, 400 
technic of, 403 

Nasal specula, 68 
Nasopharyngeal adenoids, 566 
Necrosis of inner margin of bony meatus 
in chronic middle-ear suppuration, 
202 , 211 

of ossicles in chronic middle-ear 
suppuration, 213 


608 


INDEX 


Nerves, auditory, 273 
cochlear, 272 
facial (see Facial nerve) 
glossopharyngeal, 27 
hypoglossal, 512 
Jacobson’s, 27 
trifacial, 28 
vestibular, 272 

Nervi carotid tympanici (tympanic 
branches of sympathetic), 27 
Neumann, influence of Gram negative an¬ 
aerobic bacilli upon brain tissue, 360 
statistics bearing upon usual loca¬ 
tions of brain abscess, 358 
Neumann’s operation for supurative 
labyrinthitis, 468 

Neurasthenia as a cause of tinnitus 
aurium, 142 

as an occasional cause of hyperacusis, 
142 

Noise apparatus, Barany’s, 93 
Noises as a cause of aural disorder, 131 
Non-suppurative diseases of middle ear, 
219 

Normal hearing distances for watch, acou- 
meter, conversational voice, and 
whisper, 74 

tympanic tension, loss of, 288 
Nose, examination of, 69 
Nystagmus, cerebellar, 378 

physiological, distinguishing features 
of, 283 

vestibular, characteristic features of, 
281 

types of, 282 

Objective tinnitus aurium due to aneurism 
cf basillar artery, 140 
due to aneurism of internal 
auditory artery, 140 
due to cardiac valvular 
lesion, 139 
Obliquus auriculae, 3 
Occupational diseases of ear, 130 
(Edema, postauricular, deformity result¬ 
ing from, 186 
due to furunculosis, 109 
due to suppurative mastoiditis, 
186 

Okada, statistics bearing upon etiology of 
otitic brain abscess, 357 
Opaque or covered eye-glasses, use of, in 
determining slight grades of nystagmus, 
298 

Operation for establishing faciohvpoglos- 
sal anastomosis, 511 

Operations for closing postoperative sinus 
behind ear, 459-462 
for correction of auricular deformities, 
516-525 

for cure of cerebellar abscess, 502-504 
of chronic middle-ear suppura¬ 
tion, 432-458 


Operations for cure of infective sigmoid 
sinus thrombosis, 477-489 
of suppurative labyrinthitis, 463- 
475 

of temporo sphenoidal abscess, 
490-502 

for improvement of hearing, 258 
for relief of acute purulent otitis 
media, 399-406 
of otitic meningitis, 504-508 
of suppurative mastoiditis, 409-432 
of vertigo, 475-478 

Opium, contra-indications to, in acute 
tympanic disease, 173 
Oppenheimer, S., detachment and extru¬ 
sion of ossicles in middle-ear tubercu¬ 
losis, 535 

Optic neuritis in brain abscess, significance 
of, 367 

infective sinus thrombosis (Croc¬ 
kett), 347 

Organ of Corti, 270 

function of, 277 

Organic cardiac lesions as a cause of aural 
symptoms, 139 

Orientation, mechanism of, 304 

compensatory activity of con¬ 
stituent parts of, 305 
Osseous meatus, 8 

development cf, 4 
Ossicles, 16, 213, 217, 457, 535 

disarticulation and extrusion of, in 
middle-ear tuberculosis, 535 
necrosis of, in otitis media purulenta 
chronica, 213 

Ossicular chain, position of constituent 
parts, 56 

physiology of function of, 37 
relative maximum movements of 
different ossicles, 38 

Ossiculectomy for improvement of hear¬ 
ing, 259 

on account of necrosis, 217, 457 
Otalgia (aural pain), 133 
Othsematoma, 102 
Otic ganglion, 28 
Otitic meningitis, 382 

circumscribed purulent lepto¬ 
meningitis, 385 

diffuse purulent leptomeningitis, 

383 

serous, 387 

pathways of pus to brain or meninges, 
337 

Otitis externa circumscripta acuta, 107 
externa crouposa, 118 
diffusa acuta, 116 
media catarrhalis acuta, 158 

bacteria commonly as¬ 
sociated with, 159 
etiology of, 158 
impairment of hearing 
in (Bezold), 162 


INDEX 


609 


Otitis media catarrhalis acuta 

incision of drum mem¬ 
brane in, 174 
non-operative treat¬ 
ment of, 172 
pathology of, 160 
rupture of drum mem¬ 
brane in, 161 
surgical treatment of, 
173, 399 

symptoms and physical 
signs of, 160 

hyperplastica chronica, 234 

atrophy of drum mem¬ 
brane in, 237 
paracusis Willisii in, 235 
pathology of, 234 
symptoms and signs of, 
‘ 235 

treatment of, 238 
use of Eustachian bou¬ 
gies in, 238 

hypertrophica chronica, altera¬ 
tions of tympanic ten¬ 
sion in, 228 
aural pain in, 226 
calcareous changes in 
drum membrane in, 
227 

etiology of, 223 
impairment of hearing 
in, 224 

pathology of, 223 
physical signs of, 226 
prognosis of, 229 

relaxation of drum 
membrane in, 228 
symptoms of, 224 
treatment of, 229 
purulenta acuta, antrum tender¬ 
ness in, 180 

catheter inflation in, 178 
complications of, 170 
etiology of, 165 
in infants, 169 
myringotomy in, 179, 
399 

rupture of drum mem¬ 
brane in, 167 
symptoms and physical 
signs of, 166 
treatment of, 173 
chronica, bone changes in, 
194 

central perforations of 
drum membrane in, 
201 

cholesteatomatous for¬ 
mation in, 196 
complications of, 205 
etiological relation of, to 
brain abscess, 357 
etiology of, 192 


Otitis media catarrhalis acuta 

formation of polypi in, 
194, 200 

indications for radical 
operation in, 216 
non-operative ^ treat¬ 
ment of, 205 
ossicular necrosis in, 213 
ossiculectomy in the 
treatment of, 217 
pathology of, 192 
perforations confined to 
Shrapnell’s mem¬ 
brane, 203 

physical signs of, 200 
significance of marginal 
perforations in, 202, 
211 

significance of postau- 
ricular subperiosteal 
abscess in, 216 
spontaneous resolution 
in, 195 

surgical treatment of, 
purulenta chronica, 
432 

symptoms of, 198 

Otoliths, 268 

function of, 277 
Otomycosis, etiology of, 117 
symptoms of, 117 
treatment of, 117 

Otosclerosis, Bezold’s triad symptom com¬ 
plex of, 251 

combination of, with chronic tym¬ 
panic diseases, 255 
diagnosis of, 250 
etiology of, 244 

Gray’s theory of pathogenesis of, 249 
Hartmann’s test for cochlear nerve 
involvement, 253 
pathology" of, 245 

Siebenmann’s theory of pathogenesis 
cf, 247 

symptoms of, 250 
treatment of, 255 

use of phosphorus and iodide of potas¬ 
sium in, 256 

with involvement of membranous 
cochlea, 253 

Otoscope (see Diagnostic tube) 

Oval window", 11 

Ovenvork, business strain, etc., influence 
of, upon progress of otosclerosis, 245 

Pachmeningitis, circumscribed, 382 
Page, John R., abdueens paralysis, 188 
" brain abscess successfully drained 
after multiple incisions, 498 
congenital microtia, case-report of, 517 
Panse, origin of subjective noises in tym« 
panic disease, 137 

Panse’s plastic (flap) operation, 450 


39 


(ilO 


INDEX 


Paracusis Willisii in otitic media hyper- 
plastica chronica, 235 
in otosclerosis, 252 

Parasitic inflammation of external audi¬ 
tory meatus (otomycosis), 117 
Parental consanguinity in relation to deaf- 
mutism, 562 

Parotitis, deafness resulting from, 129 
Passau-Trautmann operation, 460 
Perforation of drum membrane, diagnosis 
of, 58, 164 

epidermization of margins 
of, 193 

measures for closing, 206 
Perforations of Shrapnell’s membrane, 203 
treatment of, 214 
Perchondritis of auricle, 101 
etiology of, 101 

permanent deformity resulting 
from, 102 

symptoms and physical signs of, 

‘ 101 

treatment of, 101 
Perilabyrinthitis, definition of, 312 

differential diagnosis from other laby¬ 
rinthine lesions, 313 
symptoms of, 312 
treatment of, 320 
Perilymph, 260 

Perisinous abscess (see Abscess, peri- 
sinous) 

Perkins, C. A., abducens paralysis, 188 
Pharyngeal orifice of Eustachian canal in 

adults, 31 
in infants, 31 

Pharynx, examination of, 71 
Physical signs of acute mastoiditis, 184 
Physiology of sound-conducting appara¬ 
tus, 34 

of sound-perceiving mechanism, 274 
Pithiatism, 543 

Plastic operation for correction of ma- 
crotia, Goldstein’s, 520 
operations for closing postoperative 
opening behind ear, 459 
Mosetig-Moorhof, 459 
Passau-Trautmann, 460 
for replacement of projecting 
auricle, 521-525 

for replacement of projecting 
auricle, Duel’s, 522 
for replacement of projecting 
auricle, Ruttin’s, 522 
forming part of radical mastoid 
operation, 449 

(flap) operation, Ballance’s, 450 
BriihPs, 451 
Korner’s, 449 
Panse’s, 450 
Siebenmann’s, 450 

Pneumatic cells, wide distribution of, in 
temporal bone, 422 
mastoid, 32 


Pointing tests, in cerebellar disease, 396 
in vestibular disease, 395 
Politzer’s acoumeter, 75 

method of inflation, indications for, 61 
' technic of, 61 

Polyotia, 514 

Polypi formation of, in chronic middle-ear 
suppuration, 194, 200 
removal of, 214 

Position of membrana tympani in in¬ 
fancy, 5 

of temporal bone in infant skull, 6 
Postauricular abscess, 185 
oedema, 186 

due to furunculosis of meatus, 109 
due to suppurative mastoiditis, 
186 

opening following radical operation, 
treatment of, 459 

Posterior fold of membrana tympani, 25 
Pouches of drum membrane, 24 
Pregnancy and labor, influence of, upon 
progress of otosclerosis, 257 
Preparation of patient for mastoid opera¬ 
tion, 409 

Pritchard, osseous stapedio-vestibular 
ankylosis following middle-ear suppura¬ 
tion, 245 

Processus brevis incudis, 18 
mallei, 18 
cochleariformis, 12 
folianus mallei, 18 
lenticularis incudis, 17, 19 
Projecting ears, surgical treatment of, 517 
Promontory, 11 
Prussak’s attachment strise, 20 
space, boundaries of, 25 
Psychic blindesss (causing sensory visual 
aphasia), 335 
deafness, 543 

Quadrants of drum membrane, relation of, 
to intratympanic structures, 56 

Radical mastoid operation, 432 

Ballance’s flap operation in, 
450 

Briihl’s flap operation in, 351 
dangers of stapedial injury 
in, 441 

detailed description of, 432 
facial nerve injury and par¬ 
alysis in, 442 
indications for, 216 
influence of, upon hearing, 
455 

initial incision, 433 
Korner’s flap operation in, 

449 

Panse’s flap operation in, 

450 

postoperative treatment, 451 
-454 


INDEX- 


611 


Radical mastoid operation 

reduction of facial spur, 437 
removal of inner margin of 
canal wall, 436 
Siebenmann’s flap operation 
in, 450 

surgical treatment of Eusta¬ 
chian canal, 439 
use of skin grafts in, 453 
Rae, J. B., metastitic brain abscess second¬ 
ary to infective sigmoid sinus throm¬ 
bosis, 353 

Recessus ellipticus (fovea elliptica), 263 
sphericus (fovea hemispherical, 263 
Reduplications of tympanic mucosa, 25 
Reik, H. O., blood-clot operation, 430 
Reissner’s membrane, 270 
Resection of jugular vein in sigmoid sinus 
thrombosis, 485 

Respiratory paralysis in abscess of cere¬ 
bellum, 379 

Retraction of drum membrane, cardinal 
signs of, 147 

Retractors, self-retaining, 407 
Retrahens aurem (musculus auricularis 
posterior), 3 

Retro-auricular fistula, operations for 
closure of, 459-462 
Retzius’s fibre cells, 268 
Rheumatism and gout, etiological rela¬ 
tion of, to auricular 
eczema, 99 
to furunculosis of 
meatus, 108 
to tympanic disease, 
41 

Rhinoscopy, anterior, 70 
posterior, 71 

Richards, Geo. L., modifications of radical 
operation, 457 

Richards, J. D., initial incision in radical 
operation, 433 

operation for suppurative labvrinthi- 
tis, 467 

treatment of narrow bony meatus in 
radical operation, 443 
Richards’s curettes, 411 
Rinne’s test, diagnostic value of, 90 
method of applying, 89 
Rivinian notch, 6, 20 
segment, 6, 20 
Rods of Corti, 270-271 
Rongeur method of opening mastoid 
(Bryant), 320 
Rongeurs, selection of, 409 
Rotary nystagmus, 282 
Rotation test, diagrammatic demonstra¬ 
tions of, 302 

explanation in accordance with 
Ewald’s experiments, 283-287 
significance in diffuse suppura¬ 
tive labyrinthitis, 301-304 
Round window, 11 


Rudimentary auricle (microtia), 516 
Rupture of membrana tympani during 
inflation, 237 

in acute tympanic inflam¬ 
mation, 161 

Ruttin, eye-ground change in intracranial 
lesions of otitic origin, 366 
operation for replacement of protrud¬ 
ing ears, 516 

Saccular nerve, 272 
Saccule, anatomy of, 266 
Saccus endolymphaticus, 266 
Sagging of the posterosuperior wall of 
meatus, significance of, 184 
Salpingopharyngeal muscle, 31 
Salvarsan in relation to cranial nerve 
lesions, 548 

method of administration yielding 
best results (Fordyce), 553 
Santorini, fissures of, 4 
Satyr ear, 514 

Scala media (ductus cochlearis), 269 
tympani, 261 
vestibuli, 261 

Scarlet fever, bacteriaemia in, 354 
Scarlet fever, character and frequency of 
aural complications in, 128 
destruction of drum-head, 128 
Scarpa’s membrane, 12 
Schmiegelow, perforations of Shrapnell’s 
membrane, 204 
Schwabach’s test, 89 
Schwartze, pioneer work in mastoid sur¬ 
gery, 409 

Schwartze-Stacke operation, 432 
Sclerotic mastoid, 32 
Self-retaining retractors, 407 
Semicircular canals, anatomy of, 263 

author’s scheme for memorizing 
exact position of, 285 
experimental irritation of, 278 
physiology of, 276 
Serous meningitis, 504 

meningo-encephalitis, treatment of, 
506 

Shambaugh, distribution of labyrinthine 
blood-vessels, 273 

structural and physiological analogy 
between hair-cells of Corti’s organ 
and those of the cristae and maculae 
acusticae, 277 

theory as to function of tectorial 
membrane, 276 
Shrapnell’s membrane, 5, 21 
perforation of. 203 

Siebenmann’s plastic (flap) operation, 450 
theory as to pathogenesis of oto¬ 
sclerosis, 247 
Siegel’s otoscope, 59 

Sigmoid sinus, accidental opening of, dur¬ 
ing mastoid operation, 424 
dural walls of, 340 


INDEX 


612 

Sigmoid sinus, infection of, in relation to 
cerebellar abscess, 341 
occasional abnormal position of, 
445 

surgical exploration of, 483 
surgical exposure of, technic, 479 
Simulated deafness, tests for, 93 
Sinus, cavernous, thrombosis of, 348 
phlebitis, 343 

thrombosis (see Infective sigmoid 
sinus thrombosis) 

Skin-grafting, following radical operation, 
453 

Slinger, R. J., and Sir Victor Horsley, on 
orientation of points of space, 304 
Sound-conducting mechanism, constituent 
parts of, 1 

Sound-conduction, physiology of,JI4 
Sound-perception, physiology of, 274 
Sound-perceptive mechanism, constituent 
parts of, 1 

Sound values in conversational speech, 81 
Sourdille, war deafness, 539 
Specula, aural, 48, 49 
nasal, 68, 69 
Spine of Henle, 406 
Spiral ganglion, 269, 272 
ligament, 270 
Spur, facial, 438 

Stacke’s operation for chronic middle-ear 
suppuration, 444 
Stacke’s protector, 445 
Stapedia ankylosis in chronic hyper¬ 
trophic otitis media, 224 
fixation in otosclerosis, 246 
Stapedius muscle, division of, for improve¬ 
ment of hearing, 258 
function of, 39 
motor supply of, 28 
origin and insertion of, 24 
Stapes, anatomy of, 18 

articulation and ligaments of, 23 
extraction of, for relief of deafness, 
259 

fixation of, as result of chronic middle- 
ear suppuration, 199 
by adhesive bands in chronic 
middle-ear catarrh, 224 
in otosclerosis, 246 
maximum excursions of, 38 
mobilization of, 258 
rupture of capsular ligament, 437 
surgical injury of, as cause of sup¬ 
purative labyrinthitis, 292 
Statistics as to comparative frequency of 
temporal lobe and cerebellar ab¬ 
scesses, 358 

Korner’s, bearing upon comparative 
frequency of dural fistulce in brain 
abscess, 492 

Sterile gauze wicks in treatment of acute 
purulent otitis media, 177 
use of, in brain abscess, 501 


Streit’s operation for chronic middle-ear 
suppuration, 457 

Stucky, J. A., treatment of otosclerosis, 
257 

Subjective noises, 136 

cardiac, i.e., sounds transmitted 
from cardiac valvular lesions, 
139 

cerebral, i.e., auditory hallucina¬ 
tions due to irritation of corti¬ 
cal hearing centres, 143 
circulatory, i.e., blood sounds 
due to local vascular changes, 
138 

hsemic, i.e., a bruit sometimes 
heard in pronounced grades of 
anaemia, 140 

labyrinthine, due to organic 
changes within labyrinth, 140 
neurotic, i.e., due to hvperaes- 
thesia of acoustic nerve, 141 
tympanic, i.e., due to lesions in¬ 
terfering with sound transmis¬ 
sion, 136 

Subperiosteal abscess in acute mastoiditis, 
185 

deformity resulting from, 185 
significance of, in chronic middle- 
ear suppuration (Mygind), 216 

Sulcus tympanicus, 6 

Supernumerary nodules, auricular, 514 
treatment of, 521 

Suprameatal spine (spine of Henle), 406 

Surgical dislocation of stapes, pathological 
significance of, 315, 400, 441 
exploration of brain, 495 
guides to labyrinthine vestibule, 464 
injuries of facial nerve during laby¬ 
rinthine operation, 471 
of modiolus, pathologic signifi¬ 
cance of, 474 

measures for relief of deafness, 258 
opening (accidental) of internal audi¬ 
tory meatus, 474 

Svmptom complex of vestibular irritation, 
"287 

Symptoms of intracranial disease, 322 

Syphilis, influence of, upon progress of 
intercurrent otosclerosis, 244 
of auditory nerve, relation of salvar- 
san to, 548 

of labyrinth, acquired, 530 
congenital, 530 

Taste, disturbance of, as result of injury 
to chorda tympani nerve, 402 

Taylor, A. S., surgical treatment of facial' 
paralysis, 512 

Teeth, lesions of, as cause of aural symp¬ 
toms, 558 

Temperature and pulse changes character 
istic of intracranial disease, 324 
changes in brain abscess, 364 


INDEX 


613 


Temperature changes in infective sigmoid 
sinus thrombosis, 340 
Temporal bone, development of, 4 

relation of intracranial structures 
to, 490 

wide distribution of pneumatic 
spaces in, 422 

lobe abscess, aphasia in, 371 
bacteriology of, 359 
differential diagnosis of, from 
cerebellar abscess, 379 
etiology of, 357 
eye-ground changes in, 366 
forms of paralysis occasion¬ 
ally occurring in, 369 
mental disturbances in, 330 
operative treatment of, 490 
pathology of, 361 
postoperative treatment of, 
499 

pulse and temperature 
changes in, 365 
pupillary changes in, 371 
surgical exploration of temp- 
orosphenoidal lobe, 495 
symptoms of, 362 
technical faults in treatment 
of, 492 

terminal stage of, 374 
Tension of normal sound-conducting mech¬ 
anism, Mach’s theory, 39 
Tensor palati muscle, 31 

tympani muscle, canal for, 12 

division of, for improvement 
of hearing, 259 
function of, 39 
nerve supply of, 28 
origin and insertion of, 24 
Thompson, J. J., jugular vein, ligation of, 
477 

Throat, examination of, 69 
Thrombosis of cavernous sinus, obliterat¬ 
ing, symptoms of, 348 
of sigmoid sinus (see Infective sigmodi 
sinus thrombosis) 

Tinnitus aurium, 136 

aneurismal, due to aneurism of 
internal auditory or basilar 
artery, 140 

cardiac, sounds transmitted from 
cardiac valvular lesion, 139 
cerebral, auditory hallucinations 
. due to irritation of cortical 
auditory centres, 143 
circulatory, i.e., blood sounds due 
to local vascular changes, 
138 

hocmic, i.e., a bruit sometimes 
transmitted in pronounced 
grades of anaemia, 140 
labyrinthine, sounds due to or¬ 
ganic changes within labyrinth 
0 e.q ., in otosclerosis), 140 


Tinnitus aurium, neurotic, i.e., due to 
hyperaesthesia of auditory 
nerves, 141 

tympanic, due to tympanic con¬ 
ditions interfering with sound 
transmission, 136 
Tobacco, aural disease due to, 130 
Tobey, Geo. L., ligation of internal jugular 
vein, 489 

Tod, Hunter, ossiculectomy, for relief of 
chronic middle-ear suppuration, 458 
statistics bearing upon usual location 
of brain abscess, 358 

Tone perception, determination of changes 
in lower limit of, 83 
of changes in upper limit of, 
86 

Helmholtz’s theory of, 274 
normal limits of, 73 

Toynbee’s artificial drum membrane, 
570 

Tractus spiralis foraminosus, 272 
Tragicus, 3 
Tragus, 2 

Transversus auriculse, 3 
Trauma, 572 

Traumatic dermatitis of auricle, 97 

injuries of membrana tympani, 159 
Treatment of brain abscess drained 
through dural fistula, 494 
Trifacial nerve, tympanic branch, 28 
Tubal catarrh, acute, auscultatory signs 
of, 151 

changes in drum membrane 
in, 147 

in children, 153 
etiology of, 145 
pathology of, 145 
prognosis and treatment of, 
149 

symptoms and physical signs 
of, 146 

chronic, diagnosis of, 221 
symptoms of, 219 
treatment of, 222 

Tuberculosis of middle ear, caries of laby¬ 
rinthine capsule in, 534 
diagnosis of, 532 
etiology of, 532 
facial paralysis in, 535 
pathology of, 533 
primary, 536 
prognosis of, 536 
symptoms and physical signs 
“ of, 534 

treatment of, 537 

Tubotympanic congestion, acute, signifi¬ 
cance and phvsical signs 
of, 149 

treatment of, 153 

Tumor, acoustic, 575, 476, 578, 583 
epitome, 583 
cerebellar symptoms, 579 


614 


INDEX 


Tumor, deafness in, 578 

interval between initial stage and the 
later stage, 584 

influence of upon other nerves, 576 
of upon pons, cerebellum and 
medulla, 577 

of upon intracranial pressure, 577 
nystagmus, 580 
pain in, 579 

static and dynamic ataxia, 580 
symptoms, 578 

Tumors of the eighth cranial nerve, 571- 

586 

differential diagnosis, 585 
to epitomize, 575 
etiology, 572 
forward, 571 
pathology, 573 
terminology, 572 
failure to recognize, 571 
symptoms referable to disturbance of 
adjacent nerves, 581 

Tumors of the cerebello-pontile angle, 586 

Tuning-forks, author’s set, 86 
Bezold’s set, 86 
Hartmann’s set, 84 
use of, 83 

Tympanic cavity, anatomy of, 10 
anterior wall of, 13 
blood-vessels of, 26 
floor of, 14 

folds of mucous membrane in, 25 
inflammation of (see various 
forms of otitis media) 
landmarks of inner wall of, 11 
lining membrane of, 24 
membranous compartments of 
attic, 26 
muscles in, 23 
nervous supply of, 27 
posterior wall of, 14 
roof of, 12 
subdivisions of, 10 
muscles, function of, 39 
ring, 5 

vault, acute infection of, 166 

membranous compartments of, 26 
parts of ossicular chain in, 56 

Tvphoid fever as cause of aural disease, 
‘128 

Umbo, 19 

Unilateral muscular paralysis, interpreta¬ 
tion of, in intracranial disease of otitic 
origin, 327, 369 

Urbantschitsch, eye-ground changes in in¬ 
tracranial lesions, 366 

Utricle, anatomy of, 266 

Utricular nerve, 272 

Vaccine therapy, autogenous versus 
“stock” vaccines, 556 
in the treatment of aural disease, 
554 


Vaccine therapy, theory of, 555 

use of, in aural disease, 557 
Vagus, its communications with nerves 
controlling local blood supply of laby¬ 
rinth (Woakes), 129 
Valsalva’s method of inflation, 60 
Vein, jugular, 477, 485 
Venous sinuses of brain, chart of, 356 
Verticillium Graphii, 117 
Vertigo ab aure laeso, 528 

due to cerebellar disease, 377 
due to chronic hyperplastic otitis 
media, 236 

due to otosclerosis, 252 
due to vestibular irritation, 288-295 
due to vestibular paralysis, 303 
Vestibular apparatus, physiology of, 276 
ataxia (static), 288 
disturbances, 578 

irritation, symptom-complex of, 287 
nerve, 272 

nystagmus, characteristic features of, 
forms of, 282 

paralysis, clinical manifestations of, 
305 

Vestibule, aqueduct of, 266 
blood supply of, 273 
membranous structures of, 265 
nerve of, 272 
opening into, 263 
osseous portion of, 263 
surgical guides to, 464 
surgical technic of opening, 470 
Vomiting as a symptom of intracranial 
disease, 323 

Von Stein, percentage of cases of middle- 
ear suppuration developing labyrinthi¬ 
tis, 293 

Von Troltsch, pockets of drum membrane, 
25 

Watch-tick, normal hearing distance for, 74 
Weber’s test, value and limitations of, 90 
Whispered speech, method of testing by, 81 
normal hearing distance for, 75 
Whiting’s encephaloscope, 499 
Wittmaack’s experiments, 275 
Woakes, aural symptoms due to pelvic and 
abdominal lesions, 139 
Wolf, O., tones inherent in consonants, 81 
Word-blindness causing sensorv agraphia, 
335 

Word-deafness (sensory aphasia), 334 
Wright, Jonathan, blood cultures in sup¬ 
purative lesions of ear, 349 

Yankauer’s curette, 209 

Eustachian applicator, 240 

Zaufel-Heine opeiation for chronic middle- 
ear suppuration, 443 
Zygoma in infant and adult, 7 
Zygomatic cells, treatment of, in mastoid 
surgery, 421 
























































































































































































































































































































































































